
Class JRS_iZ 

Book .:B„1_5 

Copiglitl^" 



coPimrGHT DEPOsir. 



A TEXT -BOOK 

of 

CLINICAL DIAGNOSIS 

BY LABORATORY METHODS 



FOR THE USE OF 

STUDENTS, PRACTITIONERS, AND LABORATORY WORKERS 



L. NAPOLEON BOSTON, A.M., M.D. 

Associate in Medicine and Director of the Clinical Laboratories, Medico- 

Chirurgical College, Philadelphia; formerly Bacteriologist at the 

Philadelphia Hospital and at the Ayer Clinical Laboratory 

of the Pennsylvania Hospital 



SECOND EDITION, REVISED AND EN- 
LARGED, WITH 830 ILLUSTRATIONS 



PHILADELPHIA AND LONDON 

W. B. SAUNDERS AND COMPANY 

1905 



^ 



UBRARY of CONGRESS! 
Two Oopies rtwtiivQu 

SEP. § 1905 

Oopyrjgni tiiir^ , 
COPY '%. ^ 



^ 






Set up, electrotyped, printed, and copyrighted, August, 1904. 
and recopyrighted, August, 1 90 5. 



Revised, reprinted, 



Copyright, 1905, by W. B. Saunders & Company 



PRESS OF 
SAUNDERS &. COMPANY 
PHILADELPHIA 



THIS WORK IS RESPECTFULLY DEDICATED TO THE MEMBERS 



Sl^fociation of ^tBp-lflEsibcnt and it^egitient |0bl?sician^ 



l^bilabelpbia i^ospital 

IN APPRECIATION OF THEIR THOROUGH WORK AND 
VALUABLE CONTRIBUTIONS TO MEDICINE. 



1 



PREFACE TO THE SECOND EDITION. 



It is very gratifying to the author to be called upon to prepare 
a revision of his book eight months after its publication; and 
the favorable reception thus indicated has added stimulus to his 
effort to keep this volume abreast of modern advance. 

In this edition slight changes and additions have been made 
throughout the text and seventeen pages of new matter, covering 
the more important advances, have been added at the end. The 
additions include, among other things, such important subjects 
as Biff's New Hemogelometer; Ficker's Reaction; a description 
(illustrated) of the Leishman- Donovan Bodies; Ra void's Test 
for Albumin; Cammidge's Test for Glycerin; Cipollino's Test, 
etc. The subject of Cytodiagnosis is given more extended con- 
sideration, as practical use of this method has clearly demonstrated 
its value. References to these addenda are made at appropriate 
places in the body of the book. 

July, 1905. 



PREFACE. 



This book has emanated from a desire to satisfy the demands 
made by my pupils, and it has been prepared to meet the present 
needs of the student and of the general practitioner. 

It is hoped that the volume may prove of practical value, 
although it does not attempt to furnish more than a working 
introduction to the department of medicine under discussion. It 
is, however, designed as a practical guide, and the methods de- 
scribed are such as can be carried out with a minimum of com- 
pHcated apparatus. 

Special attention has been given to outlining in progressive 
steps the various procedures in clinical technic, such steps being 
illustrated whenever possible. Besides the detailed descriptions 
of methods of examination, the diagnostic significance of the 
clinical findings is given under special headings and is fre- 
quently accompanied by tables of differentiation. 

In the chapter on the blood the more recent methods for 
examination and staining are described and illustrated by original 
drawings; and the subject of Serum-diagnosis is carefully con- 
sidered. The protozoan parasites known to invade the blood of 
the lower animals are described in connection with the malarial 
parasite. 

In the chapter on the urine the newer methods for the estima- 
tion of sugar, Bence-Jones' albumin, uric acid, and purin have 
received consideration, and the whole chapter is illustrated by a 
large number of original half-tones and colored plates. 

An unusual amount of space is given to the consideration of 
Animal Parasites, Diseases of the Skin, Transudates and Exu- 
dates, and the Secretions of the Eye and Ear. Inoscopy and Cyto- 
diagnosis have been briefly considered. 

I am indebted to Dr. Chas. Wardell Stiles for valuable sug- 
gestions regarding the subject of animal parasites; to Dr. John 
A. McKenna, who read the proof, and to W. B. Saunders & Co. 
for special courtesies rendered while the book was in press. In 
material taken from the literature I have endeavored to give credit 
in each instance. 



CONTENTS. 



INTRODUCTION. 

PAGE 

The Microscope and Its Use 17 

The Diaphragm, 17; Light, 18; Oblique Light, 18; the Getting of Light 
with the Mirror, ig; Focus, 22; Working Distance, 22; the Condenser, 
25; Care of the Microscope, 25; Measuring of Specimens, 26; Ringing 
of Specimens, 28. 

THE BLOOD. 

Tests for the Recognition of Blood 31 

Teichmann's Test, 31; Guaiacum Test, 31. 

Estimation of the Total Volume of the Blood 31 

Haldane and Smith Method, 31. 

Study of the Fresh Blood 32 

Preparation of Slides and Cover-glasses, 32: Clinical Blood Reports, 
^^. Collection of Blood, t,t,. Immediate Examination of Blood 
and Making of Smears, 34: Immediate Examination, 34; Smears, 35; 
Life of the Blood-cells, 37. Microscopic Study of Fresh Blood, 37. 
Estimation of the Volume of the Red Cells and the Plasma, 38; Hematocrit, 
38. Estimation of the Specific Gravity, 40: Hammerschlag's Method, 40; 
Wright's Coagulometer, 41. Hemoglobin, 41: Oxyhemoglobin, 42; 
Reduced Hemoglobin, 42; Hemoglobinemia, 42; Methemoglobin, 42; 
Carbonic-oxid Hemoglobin, 43; Hematin, 43; Hematoidin, 43; Hemo- 
siderin, 43; Melanin, 43; Spectroscopic Examination of the Blood, 43; 
Corroborative Tests, 45; Dare's Hemoglobinometer, 46; Oliver's Hemo- 
globinometer, 47; Von Fleischl's Hemoglobinometer, 48; Tallquist's 
Hemoglobin Scale, 51. Counting of the Blood-corpuscles, 52: Method 
of Thoma-Zeiss, 52; Oliver's Hemocytometer, 58. Alkalinity of the 
Blood, 60. Acidity of the Blood, 64. Composition of the Whole 
Blood, 64: Albumins, 64; Peptone, 64; Inorganic Substances of the Blood, 
65; Urea, 65; Uric Acid, 65; Glycogen, 65; Fat (Lipemia) and Fatty 
Acids, 66; Glucose, 67; Diabetic Blood, 68; Acetonemia, 69; Cholemia, 
69; Biliary Acids in the Serum, 69; Globulicidal Properties of Serum, 
70; Diastatic Ferment of Blood, 70. Cryoscopy of the Blood, 70. Omostic 
Properties of the Blood, 73: Normal Salt Solution, 73. 

Study of Fixed and Stained Blood 74 

~ Slides and Cover-glasses, 74. Staining, 76: Eosin and HematoxyHn, 
76. Microscopic Examination of the Stained Blood, 77: Normal 
Blood, 77; Fixing and Staining Combined, 77; Wright's Method, 78; 
Ehrlich's Tricolor Mixture, 79. The Erythrocytes, 81. Anemia, 82; 
Chemistry of the Erythrocytes, 82. Hydremia, 83. Anhydremia, 83. 
Polycythemia, 84: Cyanosis, 84; Burns, 85; Anesthesia, 85; Effect of 
Altitude upon the Blood, 86; Polycythemia of Poisons, 88. Secondary 
Anemia, 88: Viscosity, 88; Endoglobular Changes (Simple Decoloration), 
89; Changes in Shape, Size, and Motility, 89; Atypical Staining Prop- 
erties, 90; Granular Basophilia, 91; Necrosis, 92; Megaloblasts, 92; 
Normoblast, 93; Microblast, 94; Oligemia (Quantitative Anemia), 94; 

9 



lO CONTENTS. 

PAGE 

Melanemia, 94. Normal Leukocytes, 94: Lymphocytes, 95; Large 
Mononuclears, 95; Polynuclear Forms, 96; Mast Cell, 96; Eosinophil, 
96. Leukocytes in Disease, 96; Myelocytes, 97; Transitional Neutro- 
phils, 98; Tiirck's Stimulating Form, 98; Degenerated Leukocytes, 98. 
Differential Counting of the Leukocytes, 98. Blood-plates, 100. Blood 
Dust, 100. Leukocytosis, loi: Toxic Leukocytosis, 102; Leukocytosis 
of Malignancy, 102; Leukocytosis of Anesthesia, 102; Drugs, 103; Leuko- 
penia (Hypoleukocytosis), 104; Lymphocytosis, 104; Eosinophiha, 105; 
Diminution of the Eosinophils (Hypoeosinophilia), 107. 

Bacteriology of the Blood 107 

The Reaction of Bacteria of the Blood, and their Products, 108. Method 
of Collecting Blood, 109: Films, no; Staining, no; Animal Inoculation, 
no. Bacteria of the Blood, in: Anthrax, in; Relapsing Fever, in; 
Tubercle Bacillus, 112; Leprosy, 112; Typhoid Fever, 112; Suppuration, 
113; Pneumonia, 113; Influenza, 113; Epidemic Meningitis, 114; Pur- 
pura, 114; Ulcerative Endocarditis, 114; Gonococcus, 114; Plague, 114; 
Diphtheria, 114; Fungi, 114; Malta Fever, 114; Chorea, 115; Scarlet 
Fever, 115; Scurvy, 115; Leukemia, 115. Invasion of the Red Bone- 
marrow by Bacteria, 115: Typhoid Fever, 116; Tuberculosis, 116; 
Diphtheria, 116; Scarlet Fever, 116; Erysipelas, 116. Serum-Diag- 
nosis, 116: Streptocolysis, 117. Widal Reaction, 118: Paratyphoid 
Fever, 124; Dysentery, 124; Plague, 124; Cholera, 124; Tuberculosis, 
125; Malta Fever, 125; Glanders, 125; Pneumonia, 125; Bacillus 
Pyocyaneus, 125; Fungi, 125. 

Special Pathology of the Blood 126 

Pernicious Anemia, 126. Chlorosis, 127. Leukemia, 129: Myeloid 
Leukemia, 130; Lymphatic Leukemia, 131. Pseudoleukemia (Hodg- 
kin's Disease), 132. Splenic Anemia, 132. Acute Infectious Diseases, 
133: Pneumonia, 133; Typhoid Fever, 133; Diphtheria, 135; Scar- 
let Fever, 135; Measles, 136; Small-pox, 136; Vaccinia, 137; Sup- 
puration, 137; Appendicitis, 137; Erysipelas, 138; Acute Rheumatism, 
138; Whooping-cough, 138; TonsilHtis and Serous Effusions, 138; In- 
fluenza, 138; Bubonic Plague, 139; Malta Fever, 139; Yellow Fever, 
139; Gonorrhea, 139; Actinomycosis, 139; Anthrax and Glanders, 139; 
Leprosy, 140; BacilH, 140; Takosis, 140; Hemocytolysis, 141; Purpura 
H^emorrhagica, 141; Scurvy, 142; Hemophilia, 142; Addison's Dis- 
ease, 142; Myxedema, 142. 

Parasitic Diseases Affecting the Blood 143 

Uncinaria Duodenale (Ankylostoma Duodenale), 143. Strongyloides 
Intestinalis, 143. Ascaris Lumbricoides, Oxyuris Vermicularis, Tricho- 
cephalus Dispar, 143. Trichinosis, 146. Schistosoma (Distoma, Bilhar- 
zia) Haematobium, 147. Dibothriocephalus Latus, Tsenia SoHum and 
Tffinia Mediocanellata, 147. Filariasis, 147. Dracunculus Medinensis 
(Guinea-worm), 149. Trypanosomiasis, 151: the Parasite, 151; Sleep- 
ing Sickness, 153; Animals, 153. Malaria, 153: Zoologic Affinities, 153; 
the Malarial Parasite, 157; Method of Examination, 157; Staining, 
158; HyaHne Bodies, 159; Pigmented Bodies, 159; Segmenting Bodies, 
160; Crescentic Bodies, 162; Oval Bodies, 162; Extracellular Bodies, 162; 
Flagella, 162. 

THE URINE. 

Physical Properties of the Urine 168 

Naked-eye Appearance, 168: Quantity, 168; Color, 169; Transparency, 
171; Odor, 172; Consistence, 172. Specific Gravity, 172: Increase, 172; 
Decrease, 172; SoHds of the Urine, 174. Electric Conductivity of the 
Urine, 175. Reaction of the Urine, 176: Decreased Acidity, 176; In- 
creased Acidity, 176; Alkaline Reaction, 176; Amphoteric Reaction, 177; 
Fixed and Volatile Alkalis, 177. 



CONTENTS. II 

PAGE 

Chemistry of the Urine 177 

Mineral Ash, 178. Chlo rids, 179. Phosphates, 181: Earthy Phosphates, 
182; Alkaline Phosphates, 182; Estimation of Phosphoric Acid, 184. 
Sulphates, 185: Ethereal Sulphates, 187; Neutral Sulphur, 187; Loosely 
Combined Sulphur in Urine, 187. Centrifugal Analysis, 189: Estimation 
ofChiorids, 189; Estimation of Phosphates, 190; Estimation of Sulphates, 
191 Urea, 192: Estimation of Total Nitrogen, 195, Uric Acid, 196. 
Xanthin Bases, 200. Hippuric Acid, 201. Oxalic Acid, 203: Oxalic- 
acid Diathesis, 203; Quantitative Estimation of OxaHc Acid, 204. 
Kreatin and Kreatinin, 204: Weyl's Test, 205. Proteids in the Urine, 
205: Mucin, 205; Serum-albumin and Serum-globulin in the Urine, 
206: Separation of Albumin and Globulin, 206; Douglas' Method, 206; 
Author's Method, 207; Serum-globulin, 214; Mucin (Nucleo-albumin), 
215; Emulsion-albuminuria, 216; Albumoses, 216; Peptones, 217; 
Bence-Jones' Albumose, 218; Hematuria, 221; Hemoglobinuria, 222; 
Methemoglobinuria, 223; Hematoporphyrinuria, 223; Histon, 223; 
Fibrin, 224. Carbohydrates (Sugar) in Urine, 225: Glucose, 224; Tests 
for Glucosuria, 226; Optical Saccharimetry, 236; Lactose, 238; Pen- 
toses, 238; Bail's Test, 238; ToUen's Phoroglucin Test, 239. Bile in 
the Urine, 239. Acetone, 240: Tests for Aceto-acetic Acid, 240; Tests 
for Acetone, 241. Oxybutyric Acid, 242. Diacetic Acid, 243: Ger- 
hardt's Test, 243; Arnold's Test, 243. Lactic Acid, 244. Cholesterin, 
245. Ammonia in the Urine, 246. Cystin, 246. Pyuria, 246. Alkap- 
tonuria, 247. Urein, 248. Ehrlich Diazo-reaction, 249. Ehrlich 
Dimethylamidobenzaldehyd Reaction, 249. The Volatile Fatty Acids, 
250, Fat, 251. Chyluria, 252. Ptomains, 254. Gases, 254. Effect 
of Drugs upon the Urine, 255. 

Microscopic Study of the Urine 257 

Sedimentation, 257. Microscopic Technic, 258: Light, 258; Focus, 258; 
Permanent Mounts, 258; Washing Sediments, 259; Casts, 259. Urinary 
Sediments, 260: Inorganic Sediments, 260; Uric Acid, 264; Calcium 
Oxalate, 265; Calcium Sulphate, 266; Calcium and Magnesium Soaps, 
266; Neutral Calcium Phosphates, 267; Boric Acid, 267; Tyrosin and 
Leucin, 267; Bilirubin, 270; Hematoidin, 270; Triple Phosphates, 271; 
Basic Phosphates of Magnesium, 271; Hippuric Acid, 271; Cystin, 271; 
Xanthin, 272; Cholesterin, 272; Acid Ammonium Urates, 272; Acid 
Urate of Sodium, 273; Amorphous Deposits, 274; CrystalUne Sediments 
from Alkahne Urine, 275; Amorphous Alkahne Deposits, 277. Organic 
Sediments, 278: Leukocytes, 278; Pus, 278; Epithelia, 279; Blood, 281. 
Casts (Tube-casts; Renal Casts), 283: Staining of Casts, 284; Urate 
Casts, 284; HyaHne Casts, 285; Granular Casts, 286; Blood-casts, 287; 
Epithelial Casts, 288; Pus-cells, 288; Fatty Acids, 289; Amyloid Casts, 
289; Cylindroids, 290; Floaters, 291; Spermatozoa, 291; Fragments of 
Tumors, 291. Animal Parasites, 292: Taenia Echinococcus, 292; Filaria 
Sanguinis Hominis, 294; Schistosoma Haematobium, 295; Oxyuris Vermicu- 
laris, 297; Ascaris Lumbricoides, 297; Rhabditis Genitalis, 297; Tricho- 
cephalus Dispar, 298; Anguillula Aceti, 298; Eustrongylus Gigas, 299; 
Bothriocephalus Liguloides, 300; Amoeba Urogenitalis, 300; Infusoria, 
300. Vegetable Parasites, 300: Fungi, 300; Actinomyces, 301; Aspergil- 
lus, 301; Bacteriuria, 301. 



GASTRIC CONTENTS. 

Method of Collection, 308: the Stomach-tube, 308; Washing the Stomach, 
313; Einhorn's Instrument, 314. Test-meal, 315: Ewald-Boas' Test- 
breakfast, 315; Riegel's Test-dinner, 316; Boas' Test-breakfast, 316; 
Salzer Test-meal, 316. Characteristic Features of the Gastric Juice, 317. 
Motor Power of the Stomach, 318: Leube's Method, 318; Ewald-Sievers' 



12 CONTENTS. 

PAGE 

Method, 318. Resorptive Power of the Stomach, 319. Giinzburg's 
Method for Indirectly Examining the Gastric Juice, 319. 

Chemistry of the Gastric Contents 320 

Acidity, 321: Total Acidity, 323; Amount of Hydrochloric Acid, 324; 
Source and Significance of Hydrochloric Acid, 326; Tests for Free Hydro- 
chloric Acid, 328, Ferments and their Zymogens, 335: Test for Pepsin 
and Pepsinogen, 336; Chymosin, 338. Products of Gastric Digestion, 
340: Proteid Digestion, 340; Albuminoids, 341; Digestion of Carbo- 
hydrates, 341; Digestion of Fat, 342. Fatty Acids, 342: Test for Butyric 
Acid, 343; Test for Acetic Acid, 343; Estimation of Organic Acids, 343; 
Lactic Acid, 344. Acetone, 348. Gases, 349. 

Microscopic Study of the Gastric Fluid 350 

The Vomit 352 

Odor, 352; Saliva, 353; Mucus, 353; Bile, 354; Stercoraceous Vomit, 
354; Blood, 354; Pus, 355; Parasites, 355. 

THE FECES. 

Collection of the Feces, 356. General Characters of the Feces during 
Health and during Disease, 357: Constipation, 358; Amount, 358; Form, 
359; Odor, 359; Color of Stools, 360. 

Chemistry of the Feces 362 

Reaction of the Stools, 362. Composition of the Feces, 363. Tyrosin, 
365. Fatty Acids, 367: Physical Properties of Fatty Acids, 367 Biliary 
Acids, 368. Pigments of the Feces, 369. Cholesterin, 370. 

Macroscopic and Microscopic Constituents 371 

Particles of Food, etc., 371; Mucoid, Serous, and Bloody Stools, 372; 
Epithelial Cells, 374; Blood-corpuscles, 375; Pus, 376. Intestinal Con- 
cretions, 376: Biliary, 376; Intestinal CalcuH, 377; Fatty Stools, 378. 
Crystals of the Feces, 378: Fatty Acids, 378; Charcot-Leyden Crystals, 
379; Cholesterin, 379; Hematoidin, 379; Phosphates, 379; Bismuth, 
380. Bacteria, 380: Tubercle Bacilli, 380; Pus-producing Organisms, 
381; Bacillus of Shiga, 381. 

Animal Parasites of the Feces 383 

Classification, 383. Gross Examination, 386: Microscopic Study, 387. 
Intestinal Coccidiosis, 388. Rhizopoda, 388: Amoeba CoH, 388. Flagel- 
lata, 392: Cercomonadina, 392; Tetramitina, 392; Trichomonas, 393; 
Megastoma Entericum, 394; Balantidium Coh, 395. Tape-worms 
(Cestodes), 396: Taenia Solium, 398; Taenia Mediocanellata, 399; 
Dibothriocephalus Latus, 402; Taenia Echinococcus, 404; Tsnia Mar- 
ginata, 406; Hymenolepis Nana, 406; Taenia Cucumerina, 407; Tsnia 
Flavopunctata, 407; Dipylidium Caninum, 407; Taenia Madagas- 
cariensis, 409; Taenia Africana, 409; A Questionable Intestinal Parasite, 
409; Helophilus, 410; Blue-bottle Fly, 411. Trematodes or Flukes, 
411: Fasciola Hepatica, 411; Dicroccelium Lanceatum, 412; Fasciola 
Hepatica Angusta, 412; Fasciola Hepatica ^F^gyptiaca, 412; Fasciola 
Magna, 413; Distoma Sinense, 413. Round-worms, 414: Ascaris Lum- 
bricoides, 414; Ascaris Mystax, 414; Oxyuris Vermicularis, 414; Unci- 
naria Duodenale, 415; Trichocephalus Dispar, 418; Strongyloides In- 
testinalis, 419; Strongyloides Subtihs, 421; Anguillula Intestinalis, 422; 
Trichina Spirahs, 422. 

THE SPUTUM. 
Collection 426 

Characteristics of the Sputum 428 

Microscopic Study of the Sputum 432 

Organized Constituents, 432: Fibrinous Coagula, 432; Bronchial Spirals, 



CONTENTS. 



13 



PAGE 

433; Elastic Fibers, 434. Animal Parasites of the Lung, 435: Para- 
gonimus Westermanii, 435; Bilharzia, 436; Amoeba Coli, 436; Tricho- 
monades, 436; Whooping-cough, 436; Taenia Echinococcus, 437; As- 
carides, 437; Filaria, 437. Fungi, 437. Bacteria, 438: Tubercle 
BaciUi, 438; Diphtheria, 442; Influenza, 443; Acute Bronchitis, 443; 
Chronic Bronchitis, 444; Pneumococcus, 444; Bacillus of Friedlander, 
445; Bronchopneumonia, 445; Bronchial Asthma, 445; Pulmonary 
Abscess, 445; Pulmonary Gangrene and Putrid Bronchitis, 446; Pul- 
monary Tuberculosis, 447; Incipient Phthisis, 447; Edema of the Lung, 
448; Pneumonia, 448; Organic Heart Disease, 449; Pneumoconiosis, 
449. 

Chemic Study of the Sputum 450 

Organic Substances, 450: Proteids, 451; Ferments, 451; Glycogen, 451; 
Fatty Acids, 451. 



BUCCAL SECRETION. 

Collection, 452. • Physical Properties, 452. Chemistry, 453: Sulpho- 

cyanids, 453; Sugar, 453; Diastatic Ferments, 453; Nitrates, 454. 

Microscopic Appearance, 454: EpitheHum, 454; Bacteriology, 454. 
Buccal Secretion in Disease 455 

Catarrhal Stomatitis, 455; Ulcerative Stomatitis with Angina, 455; 

Gonorrheal Stomatitis, 457; Thrush, 457; Actinomycosis, 458. 

Coating of the Tongue 458 

Tartar of the Teeth 458 

Tonsillar Membrane 459 

Diphtheria, 459; Pharyngomycosis Leptothricia, 460; Keratosis, 460; 

Cultures from the Throat, 461. 



NASAL SECRETION. 

Naked-eye Appearance, 465; Reaction, 465; Rhodan, 465; Pathologic 
Secretion, 465; Crystals, 467; Fungi, 467; Entozoa, 467. 



DISCHARGES FROM THE EAR AND EYE. 
The Ear 468 

Parasitic Inflammation of the External Auditory Canal, 469: Detection, 

469; Sterigmatocystis Candida, 469. Larvae in the Auditory Canal, 470. 

The Eye 470 

Gonorrheal Conjunctivitis, 470; Keratitis, 471; Trematodes of the Eye, 
472; Keratomycosis, 473; Keratoconjunctivitis, 473; Abscess of the 
Cornea, 474; Diphtheric Conjunctivitis, 474; Trachoma, 475; Acute 
Infectious Conjunctivitis, 475; Parasitic Cysts, 476. 



SECRETION OF THE GENITAL ORGANS. 
Semen 477 

Method of Collection, 477; Characteristics, 477; Chemistry, 478; Micro- 
scopic Study, 478. Pathology of the Semen, 480. 

Vaginal Secretion 48 r 

Microscopic Study, 481. Normal and Pathologic Secretion, 482: Gesta- 
tion, 483; Bactericidal Properties, 483; Gonorrhea, 483; Ulceration of the 
Cervix, 484; Carcinoma of the Cervix, 484; Diphtheria and Noma, 484; 
Animal Parasites, 484. 



14 CONTENTS. 

PAGE 

Menstrual Fluid 485 

Abortion, 485 ; Lochia, 485 ; Vulvitis and Vaginitis, 485 ; Pruritus Vulva, 
486; Membranous Dysmenorrhea, 486; Vaginal Blennorrhea, 486; 
Mycosis, 486; Fungi, 486. 



TRANSUDATES AND EXUDATES. 
Transudates 487 

Microscopic Study, 488: Collection, 488; Sedimentation, 489; Fixing, 
489; Staining, 489; Cytodiagnosis, 490; Renal Cysts, 490; Ovarian 
Cysts, 490; Hydatid Cysts, 491; Pancreatic Cysts, 491; Fistulous Secre- 
tions, 491. 

Exudates 492 

Serous Exudates, 492: Inoscopy, 492. Seropurulent Exudates, 492. 
Chylous Exudates, 493. Hemorrhagic Exudates, 493. Purulent Exu- 
dates, 493: Staining, 494; Gonorrhea, 494; Glanders, 497; Anthrax, 497; 
Tetanus, 497; Leprosy, 497; Animal Parasites, 497; Micrococci, 498; 
Fungi, 498. 



CEREBROSPINAL FLUID AND SYNOVIAL FLUID. 

Cerebrospinal Fluid 500 

Collection of the Fluid, 500; Staining, 502; Diplococcus IntracellulariS; 
502. 
Synovial Fluid 504 



DISEASES OF THE SKIN. 

Forms, 506; Tinea Tonsurans, 507; Tinea Trichophyton Endothrix, 
509; Tinea Circinata, 509; Tropic Tinea, 509; Tinea Barbae, 509; 
Mycotic Dermatitis (Dhobie Itch) 510; Onychomycosis, 511; Gayle, 511; 
Tinea Versicolor, 511; Erythrasma, 512; Pinta, 512; Blastomycetic Der- 
matitis, 512; Mycetoma, 512; Mpasis, 513; Vera Macaque, 514; Im- 
petigo Contagiosa, 514; Erysipelas, 515; Eczema, 515; Conditions of 
Bacterial Origin, 516; Oriental Sore, 516, 

MILK. 

Colostrum 517 

Hu:^iAN Milk 518 

Bacteria, 519. Specific Gravity, 520. Fat, 521. Proteids, 522. 



ADDENDA. 
Blood 523 

Torkritization, 523; Biff's Hemogelometer; Wetherill's Ante-mortem 
Blood Colors, 524; Polyglobulia, 524; Picker's Typhoid Reaction, 525; 
Leishman-Donovan Body, 525. 

Urine 526 

Ravold's Combined Heat and Contact Test for Albumin, 526; Clinical 
Significance of Albumin, 527; Torfugation, 528; Quantitative Estima- 
tion of Purin in Urine, 529; Quantitative Estimation of Uric Acid, 530; 
Glycerin, 531. 



CONTENTS. 



15 



PAGE 

Gastric Contents 533 

Cipollino's Test, 533; Purin Bodies in Feces, 533. 

Moisture of the Breath 533 

Clinical Significance of Buccal Secretion in Disease 534 

Cytodiagnosis 534 

Exudates 536 

Parasites of Smallpox, Vaccinia, and Varicella, 536; Protozobn of Scarlet 
Fever, 536; Chylous and Pseudochylous Fluids, 537. 

Cytologic Study of Spinal Fluid 538 

Indican in the Urine 538 



INDEX 541 



THERMOMETRIC EQUIVALENTS. 



Centigrade. 
lio° .. 
loo . . 

95 -- 
90 .. 

85 -- 
80 .. 

75 -- 
70 .. 

65 -■ 
60 .- 

55 -- 
50 .. 

45 -- 

44 -- 

43 ... 

42 .. 

41 ... 

40.5... 

40 104.0 

39-5 103-1 

39 102.2 

38-5 IOI-3 

38 100.4 

37-5 99-5 



Fahrenheit. 
,..230° 

. .212 

..203 

..194 

..185 

. .176 

..167 

-.158 

..149 

..140 

..131 

. . 122 

--113 
. . iri.2 
..109.4 
. . 107.6 
..105.8 
..104.9 



Centigrade. 

37° - 

36.5 - 

36 - 

35-5 - 

35 

34 

33 

32 

31 

30 

25 

20 

15 
10 

+ 5 
o 

—5 - 
— 10 

— i; 



Fahrenheit. 
..-98.6° 
...97.7 
...96.8 
...95.9 
...95.0 
...9.32 
...91.4 
...89.6 
,.-87.8 

..86 

■--77 
..68 

--59 
..50 
..41 
...32 

--23 
..14 

-+5 
-—4 



Centi- 
meters. 



0.54^ 
I 
2 
2-5 



I" 

1.8 
3-6 
4-5 



WEIGHTS AND MEASURES! 

1. English Weights and Measures. 

I grain (gr.). 

I ounce (oz.) =437-5 grains. 

I pound (lb.) = 16 ounces = 7000 grains 

I minim = 0.91 146 grain. 

I fluidram = 60 minims. 

I fluidounce = 8 _ fluidrams. 

I pint = 20 fluidounces. 

I gallon = 8 pints. 

2. Relations of English to Metric Systems. 



Inches, 
b 



Comparative scale 
in centimeters and 
inches. 



I grain = 64.8 

I ounce = 28.3 

I pound =453-6 

I gram = 15.432 

I kilo = 2 

I minim = 0.059 

I fluidram = 3.5 

I fluidounce = 28.39 

I pint ....=567.9 

I c.c 

I liter 

I inch 

I foot 



16.9 

35-2 

2.54 
30- " 



I yard = 91.44 



I centimeter 
I meter 



0-39 
39-37 



milligrams. 

grams. 

grams. 

grains. 

pounds 3 ounces. 

cubic centimeter. 

cubic centimeters. 

cubic centimeters. 

cubic centimeters. 

minims. 

fluidounces. 

centimeters. 

centimeters. 

centimeters. 

inch. 

inches. 



CLINICAL DIAGNOSIS. 



INTRODUCTION. 
THE MICROSCOPE AND ITS USE. 

Before attempting to use the microscope the student should 
place the instrument upon a table, in position, and examine it care- 
fully, comparing it with the illustration (Fig. i), and whenever 
necessary, he should examine the accompanying key in order 
that he be thoroughly acquainted with this complicated instru- 
ment. I am firmly convinced that the chief reason the majority 
of men fail to obtain satisfactory results with the microscope is 
that they have neglected to acquire a practical knowledge of the 
instrument, and to famiharize themselves with the technic neces- 
sary for its clinical adoption. 

In clinical microscopy the so-called compound microscope 
is required; and here it may be well to emphasize the fact that 
it is impossible to do all the forms of clinical work unless the 
microscope is provided with a two-thirds, a one-sixth, and a 
one-twelfth oil-immersion objective (Fig. 2) and a substage con- 
denser (Fig. 2). In order to use a one-twelfth objective properly 
a condenser is absolutely essential — an Abbe condenser is the 
form usually supphed (Fig. 2, E). 

THE DIAPHRAGM. 

In a modern microscope the diaphragm (Fig. 2, G) is so ar- 
ranged as to be readily adjustable. The so-called iris diaphragm 
is now employed for chnical work and has become an essential 
feature of the microscope. The particular function of the dia- 
phragm is to cut off all adventitious hght, thereby securing illu- 
mination of the object in such a manner that the hght upon 
reaching the microscope is composed of those rays that come from 
the immediate vicinity of the- object only. A diaphragm is further 
necessary in each substage in order that the aperture may be 
gaged to suit the different objectives in use, as well as the different 
2 17 



i8 



THE MICROSCOPE AND ITS USE. 



objects to be observed. Should light be received directly from 
a mirror, it is well to have the diaphragm situated as close as 
possible to the object, in order to prevent all adventitious light 
from reaching the object. Again, the diaphragm will be less likely 
to interfere with illumination from a mirror when it is near the 
object illuminated. In cHnical microscopy the condenser (illu- 
minator, Fig. 2, E) is always to be employed, and for this reason 

a further discussion of the dia- 
phragm appears valueless. 

LIGHT. 

It is not practicable to employ 
unmodified hght in chnical micro- 
scopy, and though it is preferable 
to obtain light from a northern 
exposure, this, too, is often im- 
practicable. A northern exposure, 
when the sky is covered with white 
clouds, affords a most desirable 
light, but in this cHmate the 
microscopist must complete his 
work independent of chmatic 
conditions. I have found through 
experience that a large portion of 
the microscopic study must be 
through the use of artificial light. 
A glance at figure 3 will enable 
the reader to obtain satisfactory 
Hght by carefully manipulating 
the microscope's mirror. When 
there are valid reasons for the 
operator not sitting so as to 
face the light, it is well to obtain 
light from over the left shoulder, 
as is done in reading. Light 
employed for the microscope is 
usually spoken of as reflected and transmitted, axial and obhque; 
these terms designating whether the light which illuminates a 
given object traverses such object or is reflected upon it; and 
whether or not this object is lighted uniformly or asymmetrically. 

Oblique Light. — This is hght in which parallel rays from 
a plane mirror form an angle with the optic axis of the microscope. 
Or if a concave mirror or a condenser is used, the light is oblique 




Fig. I. — I, Huygenian ocular; 2, draw- 
tube, to lengthen or shorten ; 3, main tube ; 
4, nose-piece with objectives attached ; 5, 
objective in position ; 6, stage from which 
substage is suspended ; 7, substage ; 8, ad- 
justment of substage ; 9, mirror with plain 
and concave faces ; 10, milled head of coarse 
adjustment ; 11, screw of fine adjustment. 



LIGHT. 



19 



when the axial rays of the cone of Hght form an angle with the 
optic axis (Gage). (See Fig. 3.) 

The Getting of Light with the Mirror.— i. Illumination 
is readily obtained by moving to the left the substage and con- 
denser (Fig. 2), and by placing a mounted specimen upon the 




Fig. 2.— Portion of microscope showing substage separated into three parts (C, D, E) : A, 
Objective; B, adjustment of mechanical stage; F, mirror; G, pivot to adjust iris dia- 
phragm. 

microscope stage, and employing a low objective (two-thirds) 
and a low ocular (Fig. 4). 

2. Do not attempt to illuminate the specimen until the ob- 
jective is lowered to a point about one centimeter distant from 
the object. 

3. Set the diaphragm so that its central opening is approxi- 
mately the size of the tip of the objective. 



20 



THE MICROSCOPE AND ITS USE. 



4. Manipulate the mirror (plane surface up) until the light 
is reflected through the diaphragm to the objective. 

5. Whenever the column of light has passed through the 
diaphragm, an illuminated spot appears immediately beneath 
the objective; and by looking into the microscope (Fig. 5), the 
illuminated object is seen. It is unnecessary to explain how the 




Fig. 3. — Diagram of the section of the microscope when in use, showing the rays from the 
mirror through the condenser to the object, and thence through the lenses of the objective to 
the real image and through the ocular into the eye. Dotted lines show projected rays from 
retinal image as the virtual image {A, B). 



mirror should be manipulated in order to effect this end, since 
considerable practical experience is needed. 

6. A more brilliant illumination is to be obtained through 
the use of the concave surface of the mirror, but in using this 
surface the mirror's position must be at such distance from the 
object that its focus will be at a level with the object. 



LIGHT. 



21 



7. It is my custom to advise all beginners in microscopy 
to obtain light through a low-power objective with a mounted 
specimen upon the stage of the microscope. The object which 
serves best for this purpose is a permanently mounted specimen 
of crystals of uric acid. These crystals are sufhciently large 
to be readily seen through a two-thirds objective (Plate 15), and 
possess sufficient color to render them conspicuous. 




Fig. 4. — Negative eye-piece : d, d, Focal point and diapliragm ; e, 1, eye-lens ; f, 1, field-lens ; 
e, p, rays entering cornea. 



8. The position of the substage, which also governs the posi- 
tion of the diaphragm, is of vital importance in obtaining satis- 
factory illumination, and a knowledge of this important point 
is to be obtained only through careful manipulation of the thumb- 
screw of the substage (Fig. 6), while at the same time the operator 
closely observes the effect of such manipulation upon the field and 
object under study. 



22 



THE MICROSCOPE AND ITS USE. 



FOCUS. 

By focusing is meant a bringing of the microscope and the 
object to be studied in such apposition that a clear image of the 
object is seen. It will be found that the higher the power of 
magnification, the nearer must the object be brought to the objec- 
tive. It is practical, therefore, to note that with the compound 
cHnical microscope the higher the objective, and the longer the 
microscope's tube, the nearer the objective must be to the object. 
Again, unless the oculars be par-focal, the higher the magnifica- 
tion of the ocular, the nearer must the object be brought to the 
objective. These general principles . will serve to guide the be- 




Fig-. 5.— Manipulation of substage, at same time adjusting iris diaphragm. 



ginner, though in a short time actual experience teaches him the 
distance above the cover-glass, or above the object, at which 
each objective focuses. 

Working Distance. — The distance from the object at which 
the objective of a compound microscope focuses is referred to 
as its working distance. This working distance will be found 
to vary within rather wide limits, and such variation will depend 
upon the power of magnification obtained; in other words, the 
higher the power of magnification, the shorter the working dis- 
tance. 



FOCUS. 



23 



In view of these optical conditions, the thickness of the cover- 
glass is of importance, since it may exceed the length of the work- 
ing distance of the objective employed, in which case it is impos- 
sible to focus the object. I have found that the American one- 
sixth objective has too short a working distance to focus upon 
the hnes of a Thoma-Zeiss counting chamber unless a thin cover- 
glass be employed. 

In focusing a one-sixth or an oil-immersion objective the 
technic differs but slightly: 

I. Place the shde containing the object to be studied upon 
the microscope stage, and anchor it with one of the stage clamps. 




Fig. 6.— Manipulation of fine adjustment with right hand, and substage with left hand. 
Tube extended to 160 mm. 



2. Place the head in a position so that the eye is on a level 
with the stage of the microscope, and with the right hand lower 
the tube by means of the coarse adjustment until it is possible 
to get but a faint ray of light between the objective and the superior 
surface of the cover-glass (Fig. 7). 

3. The eye is now placed in position at the ocular and the 
tube of the microscope gently elevated by means of the coarse 
adjustment. In most instances it requires but a limited amount of 
practice to enable the student to focus readily after this method. 

4. When the object springs into view, the tube is first lowered 



24 



THE MICROSCOPE AND ITS USE. 



slightly, and again elevated but a trifle, this manipulation being 

continued until a fairly clear outhne of the object is obtained. 

5. The fine adjustment wheel (see Fig. 8) should be rotated 




Fig. 7.— Position of operator in focusing. 




Fig. 8.— Manipulating fine adjustment with left hand and iris diaphragm with right hand. 



slowly, and at the same time the eye be kept in position so as 
to observe the shghtest change in the definition. 

Caution. — Do not rotate the fine adjustment wheel more than 
once. It will be found that this wheel, when rotated but a sec- 
tion of the circle, will change materially the definition (clearness 



CARE OF THE MICROSCOPE. 25 

of the object). Whenever the field of vision becomes dimmed 
to the sHghtest degree, the fine adjustment wheel should be rotated 
in the opposite direction. 

The Condenser. — The condenser (Fig. 2, E) is necessary in 
order to do satisfactory hiicroscopic work. When using the fiat 
surface of the mirror, the exact position of the condenser is not 
of special moment; but practical experience shows that it is 
possible to employ the concave surface of the mirror to reflect 
hght through the condenser; the distance between the condenser 
and the mirror, and the object, all become of importance. It is 
necessary that the operator manipulate the thumb-screw elevating 
and lowering the substage until the clearest definition is obtained 
(Fig. 6). Careful adjustment of the substage will be found of 
inestimable value in bringing out the fines bounding the squares 
of the Thoma-Zeiss counting chamber. 



CARE OF THE MICROSCOPE. 

In view of the fact that every microscope is provided with 
a small booklet giving special directions for its care, it does not 
appear to be necessary to do more than refer to the subject in 
this volume. 

The location of a particle of dirt that may obstruct or interfere 
with the view of a certain portion of the field is of practical interest, 
and will therefore be considered : 

1. First, w^hile looking at an object through the microscope 
rotate the ocular to determine whether or not the particle that 
obscures the field is rotated; and should the particle rotate, it 
is situated in the ocular. 

(a) Remove the ocular from the tube, and unscrew for a 
short distance its upper lens; return the ocular in position and 
rotate this lens, and should the dirt rotate with the lens, the superior 
lens only needs cleansing. 

(b) The above steps are appHcable to the inferior lens of the 
ocular. 

2. Particles of lint and dust may collect upon the condenser, 
and the location of such dust is determined through the fact that 
it springs out of focus and returns into focus when the thumb- 
screw of the condenser is manipulated (Fig. 6). 

3. Should the particle of dust remain unchanged after examin- 
ing both the ocular and the condenser, the student will know 
that it is situated in the objective. This point may be further 
determined by screwing the objective to about two-thirds its 
depth into the nose-piece, and then rotating the objective with 



26 



THE MICROSCOPE AND ITS USE. 



the eye at the ocular, Avhen the particle of dust Avill be rotated 
with the objective. 

Cleansing the objective, the lenses of the condenser, and the 
lenses of the ocular is of great^ importance in securing clear de- 
finition. It is customary to cleanse these lenses with a special 
paper, and under certain conditions it is allowable to moisten 
such paper with some liquid. 

Caution. — The lens nearest the tip of the objective is not to 
be cleansed with xylol, ether, or alcohol. It is my practice to 
cleanse all lenses of the microscope by the use of a silk or soft 
hnen handkerchief, moistening the handkerchief with saliva. 
Practice has shown saliva to be the most effectual medium for 




Fig. 9.— I, Ocular micrometer (natural sizej ; 2, scale of micrometer (greatly enlarged). 

the removal of oil from the objective. By moistening the finger 
TA^th saliva and sweeping over the surface of a cover-glass after 
the use of an oil-immersion objective, the oil is instantly removed 
from the cover, leaving a highly poHshed surface. SaHva is also 
a valuable solvent for Canada balsam. 



MEASURING OF SPECIMENS. 

The measuring of microscopic objects is known as micrometry. 
It would seem advisable to outhne a method bv which even 



MEASURING OF SPECIMENS. 



27 



the inexperienced may be able to determine the size of certain 
objects studied. The special apparatus necessary for this pur- 
pose is an ocular micrometer 

(eye-piece micrometer). This 
apparatus consists of a thin 
ground glass, upon one surface 
of which is placed a graduated 
scale composed of from fifty to 
one hundred lines (Fig. 9). 

The ocular micrometer is 
placed in the eye-piece upon the 
diaphragm, graduated side down. 
In the study of objects these fine 
lines appear to the eye as though 
ground upon the microscopic field. 
By rotating the ocular the gradu- 
ated scale is shifted to any por- 
tion of the field; thus it is possible to place the Hnes directly 
over the object to be measured (Fig. 10). 




Fig. lo.- 



Method of using eye-piece mi- 
crometer. 



Z' 



i 

/- 



Fig. II.— I, Stage micrometer, showing graduation at center (natural size); 2, graduation of 
stage micrometer (greatly enlarged). 



Let us suppose that it requires twenty-five of these lines of 
the graduation to equal the length of the object, a one- fifth objec- 



28 THE MICROSCOPE AND ITS USE. 

tive being employed. Remove this one-fifth objective and place 
in its stead a one- sixth objective. It will now be found that thirty 
or more of the hnes of the eye-piece micrometer are necessary 
to equal the length of the object. In other words, the number 
of Hnes required for a certain object depends entirely upon the 
magnification accomphshed by the objective employed. The 
ocular micrometer enables one to determine the length or breadth 
of a given microscopic object when this object is subjected to 
a definite degree of magnification. 

The value of a definite number of lines graduated on the eye- 
piece micrometer that were found to equal the length of a given 
object is determined through the use of a stage micrometer (Fig. 
ii). Upon the center of this glass slide is seen a graduation 
in hundredths and thousandths of an inch. The stage microm- 
eter is now to be subjected to the same degree of magnifica- 
tion that has been employed for the study of the object to 
be measured. The question of determining the measurement 
of the object in inches is but a matter of ascertaining what frac- 
tional portion of an inch on the stage micrometer is equivalent 
to the given number of lines of the ocular micrometer. This 
is best accomplished by rotating the ocular micrometer until its 
lines are parallel with the lines on the stage micrometer. 

The measurement of bacteria is scarcely practicable for 
clinical research, and the above-outlined method is given more 
particularly for the measurement of animal parasites and their ova. 

RINGING OF SPECIMENS. 

The ringing of microscopic specimens (surrounding the cover- 
glass with a narrow band of microscopic cement) is employed 
whenever it is desired that a specimen be kept for an indefinite 
period. Specimens that are to be ringed should be mounted in 
a liberal quantity of Canada balsam, in order that the balsam 
extend just beyond the margin of the cover-glass at all points 
of its periphery. The accompanying illustration (Fig. 12) will 
serve to»describe the instrument employed for this purpose. 

Anchor the slide to be ringed upon the revolving table of the 
ringer by means of clamps, care being taken to shift the slide 
so that its center is at the center of the table (see fine lines. Fig. 
12). Grasp a small camel's-hair brush between the thumb 
and index-finger of the left hand, and dip the tip of the brush 
into the microscopic cement and then rest the wrist firmly upon 
the ringer, allowing the tip of the brush to near the margin of 
the cover-glass. Hold the brush steadily, and rotate the circular 



RINGING OF SPECIMENS. 



29 



table of the ringer rapidly; then lower the tip of the brush to 
touch the margin of the cover. 

Caution. — The circular table must be rotated with rapidity, 
and a liberal amount of cement be present upon the tip of the 




Fig-. 12. — Turntable for ringiTig mounted slides. 



l)rush. It has been my custom to place the ringer upon its side 
(the shde placed in position), and to press the small wheel of 
the ringer against the moving band of a sewing-machine. 

Specimen slides ringed in this manner have been in my col- 
lection for a period of seven years. 



CHAPTER I. 
THE BLOOD. 

It is our purpose in this chapter to describe briefly the phy- 
siology of the blood, and to give in detail the technic of available 
methods for its recognition and chnical study, by which methods 
we may gain diagnostic and prognostic knowledge. Included 
will be found remarks upon the blood-changes induced by disease. 
This subject will be taken up under the following heads: 

(a) Tests for the recognition of blood. 

(b) Estimation of the total volume of blood and of its oxygen- 
carrying capacity. 

1. Microscopic study both with and 
without the warm stage. 

2. Estimation of the relation of the 
volume of the corpuscles to that 
of plasma. 

3. Ascertainment of the specific 
gravity of the blood. 

(c) Study of fresh blood : ( 4. Estimation of the time necessary 

for coagulation. 

5. Estimation of the amount of color- 
ing-matter and of the blood- 
pigments. 

6. Counting of the red and white 
corpuscles. 

7. Reaction of the blood. 

(d) Composition of the whole blood. 

(e) Ascertainment of the freezing-point (cryoscopy). 
(/) The osmotic properties of the blood. 
(g) Study of smears, dried and stained. 
(h) Bacteriologic examination of the blood. 
(i) Abnormahties of the serum and serum-diagnosis. 
(j) Special pathology of the blood. 
(k) Parasitology of the blood. 

30 



PLATE I. 



*i'^. ' ^ 

^ K I 



/ 






^ r 



•^/j 









Hemin Crystals. 



TOTAL OF VOLUME OF THE BLOOD. 3 1 



TESTS FOR THE RECOGNITION OF BLOOD. 

The most delicate and decisive test for blood is the demonstra- 
tion of the red blood-cells under the microscope, and next in order 
should be classed spectroscopic study (see Hemoglobin, page 41). 

Teichmann^s Test. — Collect a small portion of the suspected 
substance or debris, and place upon the center of a sHde; add a 
few drops of salt solution, macerate, and mix well. Evaporate 
the mixture to dryness, moisten the residue with glacial acetic 
acid, and apply a cover-glass. Heat one end of the shde gently 
over a flame (avoid boiling). While the shde is being heated, 
allow a drop of glacial acetic acid to run in from the edge of the 
cover-glass from time to time, cool, and examine under the micro- 
scope for hemin crystals (Plate i). 

Caution. — Excessive heat prevents the formation of hemin 
crystals by driving off free HCl. Too much heat also produces 
alterations in the albumins which may retard and at times pre- 
vent the formation of crystals. 

Guaiacum Test. — Prepare an aqueous solution of the sus- 
pected substance and to it add a few drops of tincture of guaiacum, 
which gives it a milky precipitate. Add a few drops of hydrogen 
peroxid (or Merck's oil of turpentine) — in the presence of blood- 
pigment a distinct blue color is immediately produced. 

Caution. — The tincture of guaiacum should be freshly made 
and diluted to the color of sherry wine. This test is capable of 
demonstrating one part of fresh blood in several thousand parts 
of water, and may be employed in the study of feces, p. 360. 



ESTIMATION OF THE TOTAL VOLUME OF THE BLOOD. 

The limits of error in the various methods for the total esti- 
mation of the blood are equally great with those of the physio- 
logic and pathologic variations, therefore it is questionable whether 
any known methods are of great chnical value. Haldane and 
Smith, however, have suggested a method which bids fair to stand 
the test of criticism. 

Haldane and Smith Method. — {a) The patient is per- 
mitted to inhale a measured volume of CO, and after three minutes 
a few drops of his blood are withdrawn for analysis, and the degree 
to which the hemoglobin is found to be saturated with this gas 
is then estimated.* 

*"Jour. of Physiology," vol. xxii, p. 232; also vol. xxv, p. 331. 



32 THE BLOOD. 

(b) The degree to which the blood has been saturated by CO 
is now known, and the quantity of this gas which may be taken 
by the whole of the patient's blood is then estimated. Let us 
suppose that 150 c.c. of carbonic oxid has been administered, 
and that the blood is found saturated to the extent of 25 per cent., 
in which case it is readily seen that 600 c.c. would have been 
required had the blood been completely saturated, or the total 
capacity for CO and Hkewise for oxygen is 600 c.c. 

(c) In order to estimate the oxygen capacity per 100 c.c. in 
any given sample of blood accurately, its color is compared with 
an equal volume of ox blood whose oxygen capacity has been 
estimated; e. g., after the patient has absorbed 100 c.c. of CO 
his blood is found to be one-fifth saturated by this gas; therefore 
the total capacity for CO or for oxygen is 500 c.c. Furthermore, 
this patient's blood is found to present the same color as that 
of ox blood, of which every 100 c.c. has been found capable of 
taking up 20 c.c. of oxygen. This patient's total oxygen capacity, 
500 c.c, when divided by the oxygen capacity of every 100 c.c, 
gives the patient's total oxygen capacity (2500 cc); we divide 
this sum by the oxygen capacity of 100 cc. of his blood, which 
is 20, and derive 25. This figure 25 is the factor for the number 
of cubic centimeters of blood in the body (2500). 

Smith, as a result of a series of estimates, gives the average 
in health as 3420 gm. In the normal cases studied he found 
this figure to vary from 2830 to 4550 gm., or in a ratio of one- 
thirtieth to one-sixteenth of the body- weight. 



STUDY OF THE FRESH BLOOD. 

PREPARATION OF SLIDES AND COVER-GLASSES. 

Both shdes and cover-glasses should be cleansed for use in 
the following manner: Place a number of cover-glasses or slides 
in a glass containing warm water and soap, when they should 
be stirred with a glass rod, after which each cover or slide is 
removed separately, placed upon a thin handkerchief, and rubbed 
gently between the thumb and forefinger. After it is thoroughly 
dried, it should be dropped into a second glass containing 
warm water. After all the covers have been transferred in this 
manner from the soap and water to the second glass, they are 
again stirred by the glass rod, and, receiving the same manner 
of treatment, are transferred to a third glass, which contains 70 
per cent, alcohol. The treatment in the alcohol should be the 
same as above outlined, after which these cover-glasses are placed 



COLLECTION OF BLOOD. 33 

in a wide-mouthed bottle containing equal parts of alcohol and 
ether, in which solution they are kept for use. 

Caution. — All cover-glasses and slides should be removed from 
the solution in which they are kept by means of clean forceps. 
They should then be dried with a soft linen or silk handkerchief, 
and placed separately in a Petri dish, the bottom of which has been 
neatly covered with a piece of filter-paper. After the desired 
number of shdes or covers have been removed, the dish is covered 
and set on a warm stage or in an incubator, in order that the slides 
may be warm when the blood is applied — a condition which 
materially facihtates securing an equal distribution throughout 
the smear. 

Clinical Blood Reports. — The following is a copy of the 
blank used by me for chnical blood reports in the Clinical Labora- 
tory of the Medico-Chirurgical College, Philadelphia: 

Name: 

Specimen Received at Laboratory: ^lo. Day Hour .]M. 

Date of Examination: 

. BLOOD EXAMINATION. 
Percentage of Hemoglobin: 
Color-index : 

Number of Red Corpuscles in i c.mm.: 
Description: 

{Normoblasts 
Microblasts 
Megaloblasts 
Number of Leukocytes in i c.mm.: 

Differential Count Based on Percentage in Corpuscles: 

Small Lymphocytes 
Large Lymphocytes 
Polymorphonuclear Neutrophils 
Transitional Forms 
Eosinophils 
Basophils 
Myelocytes 

Eosinophilic Myelocyte 
Other Forms 

Plasmodia of Malaria : 

Widal Typhoid Reaction: 

Other Serum Reactions: 

Bacteria Found (by Spreads or by Cultures) : 

Alkalinity: 

Blood-plates in i c.mm.: 

Coagulation Time: 

COLLECTION OF BLOOD. 

The points of election for the collection of blood are the lobe 
of the ear and the under surface of the finger near its tip; and the 
3 



34 



THE BLOOD. 



method to be described is employed in all clinical work except 
bacteriologic study (see Bacteriology oj Blood, page 109). 

The first step in the collection of blood is made as follows: 
Should the tip of the finger be chosen, cleanse the tip with water, 
rub gently with a soft cloth, and later moisten with ether. After 
the ether has evaporated, the finger is grasped between the thumb 
and index-finger of the left hand, and the instrument with w^hich 
the puncture is to be made, having first been cleansed wdth water 
and alcohol, is quickly plunged into the tip. The depth of this 

puncture should vary with the 
thickness of the skin (one-eighth 
to one-fourth of an inch). Gentle 
pressure may be apphed to start 
the blood flowing, after which 
four or five drops of the first 
blood exuded should be removed 
with a soft handkerchief. When the ear is chosen, the same pre- 
cautions are to be observed. The puncture may be made with 
Daland's blood-lancet (Fig. 13), which it has been my practice to 
employ, or with a new steel pen after one nib has been broken 
away. A round pointed needle should not be employed. 

Caution. — Avoid pressure, since it causes a diminished num- 
ber of the cellular elements to exude in connection with a large 
amount of serum. 




Fig. 13. — Daland's blood-lancet. 



IMMEDIATE EXAMINATION OF BLOOD AND MAKING OF 

SMEARS. 

Immediate Examination. — After the first four or five drops 
of blood have been removed by the handkerchief and a rather 
large-sized drop exudes spontaneously, the cover- glass (Fig. 14) 
(which has been warmed) is held 
by its edge between the thumb and 
index-finger, and the summit of the 
drop of blood is allowed to touch 
the center of the cover-glass, care 
being taken that the surface of the 
glass does not come in contact with 
the skin. The cover-glass is allowed 
to fall gently upon the center of a 

slide (Fig. 15), the weight of the cover-glass causing the blood 
to spread between it and the shde. 

Caution. — When pressure is used to spread the blood, reliable 
deductions cannot be drawn from the microscopic appearance of 




Fig. 14. — Styles of cover-glasses. 



EXAMINATION OF BLOOD AND MAKING OF SMEARS. 



35 



such specimens, since pressure is liable to cause distortion of the 
cellular elements. The shde may now be carried to the micro- 
scope and examined by any power objective desired. 

Smears. — When smears are to be made, the above process 
is modified only in that the cover-glass with its specimen of blood 




Fig. 15. — Glass slides (natural size). 

is allowed to fall upon another cover-glass in such a manner 
that the margin of the one projects beyond that of the other, and 
after the blood has spread, these overlapping margins are grasped 
between the thumb and index-finger of each hand and separated 
by pulling on the horizontal (Fig. 16). They are then laid upon 
a flat surface, specimen up, and allowed to dry in the air; after 




Fig. 16.— Cover-glass is touched to summit of a drop of blood and then allowed to fall on 
second cover-glass, margins overlapping ; method of separating cover-glasses. 



which they may be placed together and kept for an indefinite 
period without further treatment. 

A method which I have found more satisfactory for the be- 
ginner and for class work is to make the smears upon slides. 
The slide upon which the smear is to be made is laid upon the 
table, and a second shde is grasped between the thumb and 



36 



THE BLOOD. 



index- linger, and one edge of this slide is brought in contact 
with the summit of the drop of blood in such a manner that the 
blood collects on its under surface and edge. The second slide 
is now placed at right angles to the first (which rests upon 




Fig. 17. — Method of smearing fresh blood on the slide. 




Fig. 18. — ?t 



rcles of cedar oil or of vaselin at center of slide ; 
of blood is suspended. 



cover-glass from which drop 



the table) and so tilted as not to catch the corpuscles between 
the edge of the second and the surface of the first shde (Fig. 17); 
then it is forcibly drawn over the surface of the slide for its entire 
length. The object is to transfer the drop of blood collected 
on the edge of the second slide to the surface of the first shde by 



MICROSCOPIC STUDY OF FRESH BLOOD. 7)1 

allowing it to trail. It requires far less skill to make good spreads 
by this method than by the use of cover-glasses. 

Life of the Blood-cells. — Death of the cells may not occur 
for several hours when the cover-glass and specimen have been 
placed upon a shde as previously described; but when it is desired 
that the cell's death be deferred further, the following method 
in addition to preserving life, prevents coagulation as well as 
distortion of the cells over a much longer period. Estimating 
approximately the size of the cover-glass to be used, an incom- 
plete narrow band of cedar oil or vaselin is made upon the center 
of the shde, the oil being distributed to form two semicircles whose 
diameters are separated for a distance of one-eighth of an inch 
(Fig. 1 8). The cover-glass containing the blood is now allowed 
to fall, specimen down, upon the oil, when by its weight the oil 
from the two hemispheres is forced to unite, forming a complete 
ring, hermetically seaHng the specimen. 

Caution. — A complete ring of vaseHn causes more air to be re- 
tained with the specimen and thereby favors destructive changes. 

In studying the various animal parasites of the blood this 
method is most satisfactory, and is also useful in studying rouleaux 
formation. The filaria and the malarial organism may in this 
way be kept alive for a long time. 



MICROSCOPIC STUDY OF FRESH BLOOD. 

Fresh blood collected for study in either of the methods pre- 
viously described may be placed on a warm stage or in an incubator; 
or, better still, upon the microscope, w^hich is placed wdth its 
specimen in a warm oven and removed from time to time for 
examination. 

The character of the blood as it exudes from the incision is 
worthy of special consideration, since it flows more readily than 
usual in such conditions as peripheral congestion, vasomotor 
dilatation, decided fluidity of the blood, chlorosis, certain anemias, 
and hemophiha. Blood usually flows sluggishly in such con- 
ditions as extreme anemia (primary or secondary), after hemor- 
rhage, diarrhea, cholera, exposure to cold, hysteria, uremia, vaso- 
motor spasm, and in increased coagulabihty. 

Microscopically we may detect the Plasmodium malari?e, 
Filaria sanguinis hominis, spirochaete of relapsing fever, trypano- 
soma, Piroplasma hominis, and rouleaux formation. Again, but 
with far less accuracy, we may determine whether the blood contains 
an excess of fibrin, whether there is decided anemia, leukocytosis, 
or a deficiency or excess of hemoglobin; we may make an approxi- 



38 



THE BLOOD. 



mate estimation of blood-plates, and determine whether the red 
cells display any abnormality as to size and form. It requires 
a thoroughly skilled microscopist to detect with certainty the 
existence of these latter named conditions, and perfection in this 
particular can be attained only by actual experience. The ame- 
boid movements of the leukocytes and the malarial parasite, 
the irregular contraction of dying protoplasm, which causes false 
motions in certain of the crenated points of normal red cells, 
and the Brownian movement of the protoplasm of corpuscles, 
must be carefully distinguished. Language seems inadequate 
to describe these differences definitelv. 



ESTIMATION OF THE VOLUME OF THE RED CELLS AND THE 

PLASMA. 

This is accomphshed by means of the hematocrit, which was 
first suggested by Blix, and has undergone several modifications; 
until the present instrument, as suggested by Judson Daland, 
appears to meet the demands necessary for clinical investigation. 
Its direct object is to ascertain the relative volume of the corpuscles 

and of the plasma in a given quantity 
of blood. IMany of its advocates, 
however, contend that it will replace 
the Thoma-Zeiss instrument in the 
estimation of the red cells, but as 
yet it has not displaced this instru- 
ment in either foreign or American 
laboratories. It must be admitted 
that Daland's claims for the instru- 
ment are correct, and that for chnical 
purposes the red cells can be closely 
estimated with sufficient accuracy, 
except in cases where a high grade 
of leukocytosis exists (leukemia). 

The im.proved electric centrifuge 
consists of an iron-clad motor (Fig. 
19) carrying an armature or horizontal bar, which may be re- 
placed by the bar of the hematocrit (Fig. 20). A speed indicator 
should also be attached which strikes a bell every 100 revolutions, 
and a rheostat employed to control the current and speed. A speed 
of 8000 to 10,000 revolutions may be obtained by the street- 
current or from a small battery. The centrifugalizing should 
be continued for from two to four minutes. Less satisfactory 
results are to be gained by the employment of the hand centrifuge 




Fig. 19. — Electric centrifuge with rheo- 
stat. 



VOLUME OF THE RED CELLS AND THE PLASMA. 



39 



(Fig. 2i). The hematocrit armature contains two capillary tubes, 
which are held in position by springs (Fig. 20). 

Process. — When it is possible for the patient to come to 
the laboratory, fresh blood is used. The capillary tubes are 




Fig. 20. — Daland's armature of centrifugal machine (hematocrit). One tube in position. 



removed from the armature and filled by holding the tube hori- 
zontally and touching its tip to the summit of a rather large drop 
of blood. It is then inserted into the armature as seen in figure 
20, the opposite tube filled with water, 
and the centrifugalizing begun before 
the blood has had time to coagulate. 

In estimating the blood of patients 
situated at a distance it is necessary to 
dilute the blood in a 2.5 per cent, solu- 
tion of potassium bichromate (Daland). 
A dilution to one-half with this solution 
is accomphshed by using either the white 
cell or the red cell pipet of the Thoma- 
Zeiss hemocytometer. In this instance 
it may be well to fill both tubes of the 
hematocrit with diluted blood. Healthy 
blood after it has been centrifugalized 
for from two to four minutes will show a 
sediment registering at about 50 per 
cent, (graduation on the tube of the 
hematocrit). One per cent, represents 
about 1,000,000 red corpuscles, and, 
therefore, it is necessary to add five 
ciphers to the percentage volume found, 
thus obtaining the number of red cor- 
puscles in I c.mm. of undiluted blood; 
e. g., suppose the reading on the gradu- 
ated tube (see Fig. 20) is 40, multiply this figure by 100,000, which 
equals 4,000,000, the number of red cells in i c.mm. of undiluted 




Fig. 21. — Hand centrifuge. 



40 THE BLOOr. 

blood. The leukocytes often form a thin band at the central end 
of the column of red corpuscles and should no: be included in the 
reading. 

Daland in working with diluted blood concludes that the 
number of cells for each degree of the scale should be placed at 
99,390 — practically 1 00.00c. AVhen undiluted blood is used in 
the estimation, there appears to be greater liabihty to error. The 
size of the red cells differs widely in the various forms of anemia, 
and such differences must influence the readings obtained by the 
hematocrit. 

P^or description of Wetherill's Torkrit see p. 523. 

ESTIMATION OF THE SPECIFIC GRAVITY. 

The most available method for clinical use is that sus^srested 
by Hammerschlag. "^ Avhich is a modification of Roy's f method. 

Hammerschlag's Method. — Two solutions (chloroform and 
benzol) are to be mixed in a urinometer glass in such proportions 
that the specific gravity, taken by an ordinary urinometer, is 
1.059, c>^ ^^'^^^ ol nomial blood; the former of these solutions being 
heavier than blood, the latter lighter. The finger is punctured, 
a drop of blood is collected in a Thoma-Zeiss pipet, and a drop or 
two blown into the chloroform-benzol solution. The blood 
shows no tendency to mix with this solution, but floats as a ruby 
bead. Should the beads sink to the bottom, chloroform is added, 
and should they rise to the top, benzol is added drop by drop 
until the blood remains stationary in the body of the liquid. 
Since the specific gravity of the blood is that of its surrounding 
mixture, take the specific gravity of this hquid by means of an 
ordinary urinometer and the graduation figure obtained equals the 
specific gravity of the blood. 

Caution. — ^Add chloroform or benzol a few drops at a time, 
stirring with a glass rod after each addition. A^-oid having any 
air with the drop of blood. Rapidity is necessary; and a urin- 
ometer with a scale graduated to 1.070 is best for this purpose. 

The specific gravity of the blood has been found to bear certain 
parallels with the percentage of hemoglobin, yet this may not be 
constant. The specific gravity of the plasma varies but Httle except 
in dropsy, and in the corpuscles themselves the variable element is 
the hemoglobin. In most non-dropsical patients the specific gra\-ity 
of the whole blood bears a more or less direct relation to the 
hemoglobin. In leukemia the specific gravity is relatively higher 
than the hemoglobin, and is dependent upon the weight of the 
leukocytes; while in pernicious anemia, where a high color- 

*"\Vien. med. Wochensch.,*' iSqo, vol. iii., p. iciS. 
t " Proceedings Phys. See," 18S4. 



HEMOGLOBIN. 



41 



index is to be found, the hemoglobin is slightly higher than one 
would gage it from the specific gravity. The accompanying 
table will enable one to estimate the value of a given specific 
gravity in per cent, of hemoglobin, according to Schmaltz: 



Spec. Gra> 
1.030 

1-035 
1.038 
1. 041 
1.0425 



Hemoglobin. 
20 per cent. 
30 

35 
40 

45 



Grav 



1.059 



Spec 

I -045 5 
1.048 
1.049 
1.052 
1.056 
100 



Hemoglobin. 

50 per cent. 

55 
60 

70 
80 



Wright's Coagulometer. — This instrument (Fig. 22) is 
composed of a central metal cyhndric can, surrounding which 
is a closely fitting leather case containing nine small pockets, each 
lined with flannel. One of these pockets holds a thermometer 
graduated to 50° C. (Fig. 22). The remaining pockets serve as 
receptacles for the capillary blood pipets. Each 
pipet is composed of clear glass, is about 10 cm. 
in length, and has a lumen of 0.25 mm. 

Method. — I. Fill the cyhnder with water at 
the body-temperature (37° C. — 98!° F.). 

2. Label the tubes a, b, c, etc., and place 
them in the pockets, and when they are warmed, 
obtain a rather large drop of blood from the tip 
of the finger and from it fill, by aspiration, tube 
(a) to one-half its capacity and immediately 
place this tube in its pocket. 

Caution. — Note the time of filhng tube la- 
beled (a) and also record the condition of its 
blood when examined three minutes later. 

3. In a like manner several of the tubes are 
filled with blood at intervals of one minute. 

4. Remove the tubes from the instrument at 

different lengths of time after the blood has been withdrawn, 
and endeavor to force the blood from the tube by blowing. The 
time necessary for the blood to clot in the tube is regarded as 
the coagulation time. 

Cleansing the tubes is accomphshed by passing a fine wire 
into the tube and breaking the clot, after which the tubes are 
washed with water, alcohol, and lastly with ether. 

For description of Biff's Hemogelometer see p. 523. 

HEMOGLOBIN. 

This proteid contains nearly 96 per cent, of albumin and 4 
per cent, of pigment (hemochromogen). In the red cells hemo- 




Fig. 22. — Wri£,-ht's 
coasrulomeler. 



42 THE BLOOD. 

globin probably exists in combination with the nucleoproteid of 
the stroma. The characteristics of this union are not understood, 
yet it certainly renders hemoglobin practically insoluble, con- 
centrated, and capable of forming with great rapidity indefinite 
compounds with oxygen. The chemic composition of hemoglobin 
is both complex and variable. Its spectroscopic relations, how- 
ever, are constant; and while in the circulation it exists in the 
veins principally as reduced hemoglobin; and in the arteries, 
on account of molecular union with oxygen, as oxyhemoglobin. 
Each gram of saturated oxyhemoglobin contains 1.16 c.c. of 
oxygen, but this degree of saturation varies greatly. Blood 
titrated with a standard solution of tartaric acid does not give the 
characteristic absorption-bands of oxyhemoglobin, methemoglobin, 
and carbon-monoxid hemoglobin after the alkalinity is neutrahzed 
(Dare). 

Oxyhemoglobin is non-diffusible, of a bright red color, and 
while it crystalhzes with difficulty, may form yellowish-red rhombic 
plates which are readily soluble in water and in weak solutions of 
the alkaline carbonates. They are insoluble in strong alcohol, 
ether, carbon disulphid, benzol, and chloroform. Labbe * found 
an increased quantity of oxyhemoglobin in the new-born, ranging 
from 15 to 16 per cent. During the first ten days of extra-uterine 
life it falls to 14 per cent. Such bloods likewise contain a high 
percentage of reduced hemoglobin. 

Reduced hemoglobin is of a dark cherry-red color, but after 
high dilution it may display a greenish tint. It is not readily 
crystalhzed, but is more freely soluble than is oxyhemoglobin. 
It is demonstrable in the blood of asphyxia and in the new-born. 

Hemoglobinemia (hemocytolysis) is a condition charac-, 
terized by a solution of the hemoglobin in the plasma; and in 
man is a pathologic condition which probably results from lowered 
vitality of the erythrocytes, and also from abnormahties in the 
plasma (see Viscosity, page 88). Diminished resistance of the red 
cells may be found to accompany the hemoglobinemia following ex- 
tensive burns (see Isotonic Tension, page 73), while the hemoglo- 
binemia seen after poisoning may, in part at least, be due to 
changes in the serum. 

Methemoglobin displays a brownish-red color, and crystal- 
lizes as brownish-red needles, prisms, and hexagonal plates. It 
is readily soluble in water and contains about the same proportion 
of oxygen as oxyhemoglobin, but the oxygen appears to have 
formed a rather firm union. It is observed in connection with 
poisoning. 

*"Re\aie de medecine," Dec. 10, 1900 (2ome Annee, No. 12). 



HEMOGLOBIN. 



43 



Carbonic-oxid hemoglobin is the name given to hemoglobin 
containing CO, which gives the blood a rose-red or bluish color. 
Its crystals display a slight bluish tint, and are not easily dissolved. 
It is met with after poisoning by the inhalation of illuminating 
gas, and may remain in the blood for a period of several days. 

Hematin (Plate i) appears in the feces after gastro-intestinal 
hemorrhage, in bloody transudates and effusions, and in the urine 
after poisoning with arsenic. 

Hematoidin is a derivative of hemoglobin, and appears either 
as needles or rhombic plates which are of a hght- or dark-orange 
hue, soluble in ether, carbon disulphid, ammonium disulphid, and 
chloroform. It absorbs most of the violet end of the spectrum, 
but does not contain iron (Fig. 24). 

Hematoidin occurs in bloody exudates of long standing and in 
the urine after traumatism to the kidney (Yarrow). (See Plate 17.) 

Hemosiderin results from the destruction of hemoglobin; is 




Browning's spectroscope. 



amorphous, and occurs in the viscera after exteTisive blood de- 
struction. 

Melanin is a yellowish-brown or black pigment, insoluble in 
water, alcohol, chloroform, ether, and weak acids. It is soluble 
in strong alkalis, destroyed by heat, and does not give reactions 
for iron. It results from the action of the malarial parasite upon 
the hemoglobin, and should be distinguished from other pigments 
which may or may not contain iron, and whose origins are un- 
known. 

Spectroscopic Examination of the Blood. — Spectroscopic 
examination of the blood serves as the most reliable test for the 
recognition of blood pigments, and also for the determination of 
the particular form of pigment. A one per cent, solution of fresh 
blood is found to produce distinct absorption-bands, and when 
the blood has become dried, it is necessary to dissolve it by macer- 
ating in acetic acid. With such blood the spectrum of acid 



44 



THE BLOOD. 



hcmatin is obtained. Blood from recent clots may be dissolved 
in water. When heat has been applied to the blood, macerate in 
a solution of ammonia, when the spectrum of reduced or alkaline 
hematin appears (Fig. 24). Browning's spectroscope (Fig. 23) 
will be found satisfactory when strong daylight or gaslight is em- 
ployed. A collar serves to enlarge or diminish the aperture, and 
will be found necessary in different strengths of Hght ; also when 
fluids of different opacities are used. Fraunhofer's lines are 
brought into focus by careful adjustment of the tube. Fluid to 





Red. 




Grantee. 


Vellow. r, 


reen. 


Bhie. Indi 


?o. 


J 


\ a 


] 


i L 


L 


) t 


: 


J 1- 


G 

! 


Oxyhemo- 
globin. 


















1" 
i 
























1 
















' Reduced 

Hemoglobin. 




















f. 










• 

j ■ , 






Reduced 
Hematin. 

Methemoglobin 
Acid. 












1 
















.._ _ L 














I 1 








i 


J 




1 

i 




t'k 


CO-hemoglo- 

bni. 
























f 






. 













Hematin 
Alkaline. 














■ 
















1 ,;!,; 








i: 


At id Hemato- 
porphyrinuria. 




L 












L 




L 






1 :• ■ 

i i ■ 

— L ._ i i 




c 


,\!kaline Hema- 
t <)porph\rin- 

uiia. 



Fig. 24. 



-Diagram of the spectra of eight substances known to concern us from a diagnostic 
standpoint. 



be examined should be placed in small glass vials with flattened 
surfaces. The spectrum of fresh arterial blood is that of oxyhemo- 
globin, and shows two absorption-bands between D and E (Fig. 
24) : one of these is sharp, dark, and well-defined near the orange, 
D; the other is wider, less sharply defined, and rests near the 
green, E. The indigo and most of the blue will be absorbed, and 
in strong solutions of oxyhemoglobin these two bands may unite. 
In case ammonium sulphid is added to such solutions, the 



HEMOGLOBIN. 45 

color of the fluid becomes dark, and the spectrum changes to that 
of reduced hemoglobin, when one band of absorption occurs be- 
tween D and E (Fig. 24). A positive indication of the presence 
of blood is that the spectrum may be transformed from that of 
oxyhemoglobin to that of reduced hemoglobin by the addition of 
reducing agents to the solution. Cochineal and ammoniated 
carmin give spectra simulating that of oxyhemoglobin. The 
addition of boric acid to a solution of these substances causes 
their spectra to be displayed by the blue, while the spectrum of 
blood is unchanged. Other of the vegetable dyes have spectra 
simulating those of blood, but these become pale upon adding 
sodium bisulphite. 

Methemoglobin. — Hematin is produced by adding acids or 
strong alkahs to reduced hemoglobin. In acid solution its spec- 
trum simulates that of acid methemoglobin, while in alkaline solu- 
tion it gives a broad band at D (Fig. 24). A chnically important 
change is that of oxyhemoglobin into methemoglobin, which is 
detected by the chocolate color of the blood, and in acid or neutral 
solution it gives four absorption-bands: one rather distinct between 
C and D ; a second faint narrow band in the yellow just to the 
right of D ; a third broad, fairly distinct band between the yellow 
and the green just to the left of E; and a fourth broad band to 
the left of F, which sometimes extends beyond the Hne F into the 
blue. 

Carbonic-oxid-hemoglobin is detected in cases of poison- 
ing by illuminating gas, and to the naked eye is of a rose-red color 
in both arterial and venous blood. A one-half of one per cent, 
dilution of such blood gives a spectrum that differs from that of 
oxyhemoglobin only in that its bands are broader and that the 
band at D is displaced to the right. The addition of ammonium 
sulphid causes the spectrum of oxyhemoglobin to be replaced by 
that of reduced hemoglobin, while that of carbonic-oxid-hemo- 
globin is unchanged. 

Corroborative Tests. — Prepare a two per cent, solution of 
blood and to it add a few" drops of orange-colored ammonium 
sulphid containing an excess of sulphur; add a few drops of dilute 
acetic acid, and shake gently to effect a mixture. Carbonic-oxid 
blood is recognized by displaying a rose-red color, and disseminated 
throughout the mixture are seen floccuH; while normal blood 
assumes a greenish or reddish-gray color. This test may be 
accomphshed in a test-tube. A dilute solution of zinc chlorid or 
of platinum chlorid gives a bright-red color w^ith carbonic-oxid 
blood, while normal blood is changed to black. By diluting the 
blood solution four or five times with acetate of lead, carbonic- 



46 



THE BLOOD. 



oxid blood changes to red, while normal blood becomes chocolate. 
Diluting a neutral solution of carbonic-oxid hemoglobin, a clear 
red coagulum results; while oxyhemoglobin turns grayish-brown. 
Warming the blood with an equal amount of a lo per cent. XaOH 
solution, normal blood becomes a dark brownish green; while 
carbonic-oxid blood is first cloudy, later clear red, and red flocculi 
gather on the surface. 

Dare's Hemoglobinometer. — This instrument was devised 
by Arthur Dare, of Philadelphia, for the purpose of registering 
the percentage of hemoglobin in the undiluted blood. For color- 
imetric observations with this instrument the drop of blood is 





Fio^. 25. — Dare's hemoglobinometer. 



collected by capillary attraction into a chamber of definite thick- 
ness and of sufficient surface for a color field. Illumination is 
effected by candle light. Between the stratum of blood and the 
flame of the candle a white glass slide is interposed to diffuse the 
direct rays of Hght. The color of the blood is compared with a 
graduated color prism — a tinted glass which represents the hemo- 
globin in the blood examined. The blood pipet (Fig. 25, D, A, B) 
when filled is placed into a special receptacle upon the side of the 
instrument and directly between the eye-piece and the flame of the 
candle. After the candle flame (Y) and the capillary pipet (W) are 
properly adjusted, the eye-piece (U), which is telescopic, is adjusted 



HEMOGLOBIN. 47 

to accommodate the observer. The color prism is changed by 
using the milled wheel (R) at the top of the instrument. By this 
instrument the hemoglobin is estimated in a much shorter time 
than can be done by any other hemoglobinometer, and after one 
has become thoroughly proficient in reading color with one eye 
closed, and accustomed to the necessary variations, I see no reason 
why Dare's instrument should not be considered a valuable addi- 
tion to our chnical laboratory apparatus. 

I have studied the blood from a large number of patients from 
the Medico- Chirurgical Hospital Dispensaries, correlatively using 
this instrument with that of von Fleischl and of Ohver, and while 
the readings obtained by Dare's instrument have not at all times 
agreed with those obtained by the other instruments, its registra- 
tion has always been sufficiently close to enable me to recommend 
it to the profession. Contrary to the statements commonly 
heard concerning Dare's instrument, my experience shows that 
it requires more time and attention to detail to teach the student 
to estimate hemoglobin with this instrument than with the other 
instruments considered. From ten to twelve seconds should be 
the time for observation. 

Oliver's Hemoglobinometer. — OHver's instrument enables 
us to estimate more closely the percentage of hemoglobin than 
has hitherto been accomplished by other instruments devised for 
this purpose. It consists of a series of 12 stained-glass discs, 
corresponding to the hemoglobin percentages from 10 to 120, 
which are arranged in two rows (Fig. 26). This instrument as 
used for general chnical work has two riders, a lighter and a 
darker. Intermediate shades are measured by means of colored 
glass riders which are placed on top of the primary color disc to 
deepen the tint seen, and make it correspond to that of the grad- 
uated colored disc. A capillary pipet (Fig. 33, a) is used to collect 
the blood, which is washed into the mixing cell (Fig. 26, e) by 
means of a medicine dropper provided with a rubber tube to fit 
over the blunt end of the pipet. The mixing cell is filled to the 
brim with distilled water and covered with a small glass plate. 
The bubble which forms underneath this plate should be small, 
and the cell so turned as to prevent any shadow^ upon the color 
field. The cell is now brought close to the scale and compared 
with the tints of the different standard discs. Should it match 
one of these, the observation is complete. Should it not, one of 
the glass riders, capable of reading within 2 J degrees, is placed 
upon the chamber, and the particular disc it matches noted. It 
may be necessary to apply more than one rider, and if desired 
riders may be obtained which register a single degree. The 



48 



THE BLOOD. 



Standard was originally arranged for candle light, and discs stand- 
ardized for reading by daylight are seldom used. The outer light 
is excluded by the use of a hydroscope tube; the matching of 
colors is quite simple and does not require special description. 




Fig. 26.— Oliver's hemoglobinometer : a, Colored discs ; e, mixing chamber. 



Von Fleischl's Hemoglobinometer. — This instrument con- 
sists of a stand which somewhat resembles the base and table of 
a microscope; a ground cyhnder, which is divided into halves; a 



HEMOGLOBIN. 



49 



plaster-of-Paris reflector; a graduated color prism; a thumb- 
screw adjustment; and a capillary tube (Fig. 27). 

Method oj Application. — i. One compartment of the grad- 
uated cyhnder is half filled with distilled water, care being pre- 
viously exercised to cleanse the chambers of the cylinder. 

2. The capillary tube, which has been previously cleansed 
and dried, is held upon the horizontal and brought into contact 




Fig. 27. — Von Fleischl's hemoglobinometer : a, Stand ; b, narrow wedge-shaped piece of 
colored glass fitted into a frame (c), which passes under the chamber; d, hollow metal 
cylinder, divided into two compartments, which holds the blood and water; e, plaster-of- 
Paris plate from which the light is reflected through the chamber; f, screw by which the 
frame containing the graduated colored glass is moved ; ^, capillary tube to collect the blood ; 
h, pipet for adding the water ; z, opening through which may be seen the scale indicating per- 
centage of hemoglobin. 



with the summit of a drop of blood. It fills immediately by 
capillary attraction. All blood cHnging to the outer surface of 
the tube is removed by a soft handkerchief, and the tube immersed 
in the distilled water contained in the cyhnder. It is held hori- 
zontally, shaken gently until apparently emptied, when a few 
drops of distilled water are forced from a dropper through the 
tube in order to wash every particle of blood into the cylinder. 
4 



50 



THE BLOOD. 



3. After the expulsion of the blood stir the solution gently 
with the metal handle of the pipet to effect a perfect mixture. 

4. By the use of a dropper fill both compartments of the 
cylinder to the brim with distilled water. Moisten with the 
breath the ground cover-glass, and then allow it to fall gently 
upon the cyhnder, when there will appear two small bubbles, one 
upon each side of the partition. Should the bubble upon the side 
containing the blood be large, it is evident that sufficient diluting 
fluid has not been added and that our reading will be too high. 




Fig. 28. — Estimation of hemoglobin by von FleischTs instrument, showing position of instru- 
ment, candle, and operator. Left eye closed, reading with the right only. 



When too large an amount of distilled water has been added, the 
solution containing the blood may be forced across the partition 
to mingle with the clear water on the other side, this again de- 
feating our purpose. 

5. With the cover-glass properly adjusted, turn the cylinder 
so that the portion containing the blood will be toward the light; 
thus the portion of the cyhnder containing only distihed water is 
over the graduated color prism. 

6. A dark room is necessary in this estimation, and the candle 
should be placed directly in front of the instrument (Fig. 28), 



HEMOGLOBIN. 



51 



*»<\ 



and the plaster-of-Paris mirror so adjusted as to bring the column 
of Hght through the solution. 

7. The operator should stand at the side of the instrument, 
bringing his face directly over it, and should read with the eye 
that is farthest from the light (Fig. 28) (all direct light from the 
candle should be obstructed from the eye by holding some object 
to the anterior edge of the instrument). This may be accom- 
plished by rolling a paper in the form of a tube. I have not 
been able to acquire satisfactory results by reading with both eyes. 

8. Use the thumb-screw with rather short and quick turns, 
since it is difficult to detect the 

changes in the color of the prisms 
when it is slowly moved. 

9. When the percentage of color- 
ing-matter is suspected of being 
extremely low, two or more pipet- 
fuls of blood should be placed in 
the solution. It is impossible to 
estimate with any degree of accu- 
racy when the reading is below 
40 per cent. In teaching I have 
found that in a section of twelve 
students there is seldom a difference 
of twelve points (12 per cent.) in 
the readings they make after they 
have been privileged to use this 
instrument the third time. The 
wide scope of errors so commonly 
observed by others has not been my 
experience in using von Fleischl's 
instrument. 

Tallquist's Hemoglobin Scale. — Tallquist has devised a 
color scale which is accompanied by a booklet containing small 
sheets of a special paper. The color scale is graduated from 10 
to 100. Touch the summit of a rather large drop of blood with 
the paper, and as soon as the blood has been distributed over that 
portionof the paper which it will occupy the paper is laid beside 
the color scale, and moved to a point where it matches one of 
the color blocks (Fig. 29). I have found this method fairly satis- 
factory for the average chnical work, and am of the opinion that 
the person with limited experience obtains better results by this 
simple method than by those more elaborate methods previously 
described. For description o^ Wetherill's color tests see p. 524. 



wf 


-, / 


-■'-./*, 


^-iiuyi 



Fig. 29.— Tallquist's hemoglobin scale. 



52 THE BLOOD. 



COUNTING OF THE BLOOD-CORPUSCLES. 

Method of Thoma-Zeiss. — Among the many instruments 
devised for this purpose that of Thoma-Zeiss with possibly 
Zeppert's modification of the ruhng of its counting chamber is 
doubtless the best. The use of the Thoma-Zeiss instrument is 
executed in the following manner: 

I. The cleansing of the part for the puncture and the securing 
of a proper drop of blood are obtained as previously described (page 
34). In addition it is necessary that the blood be diluted for this 
purpose and one of the following solutions is to be employed : 

(a) Hay em's solution: 

Mercury bichlorid 0.5 gm. 

Sodium sulphate 5.0 

Sodium chlorid — 2.0 " 

Distilled water. 200.0 c.c. 

(b) Toisson's mixture: 

Methyl-violet 0.025 g'^''- 

Sodium sulphai J 8.0 " 

Sodium chlorid i .0 " 

Pure glycerin 30.0 c.c. 

Distilled water 160.0 " 

These solutions will preserve the red cells for twenty-four 
hours, and their specific gravities are such that the cells precipitate 
slowly. Toisson's solution stains the leukocytes a violet tint. 
These solutions keep well, but should be filtered whenever they 
display the slightest clouding. A one-half of one to two per cent, 
solution of acetic acid is used as a diluent when we desire to count 
the white cells. It is to be remembered that acetic acid decol- 
orizes the red cells. 

The pipet for the counting of the red cells consists of a glass 
rod with an expanded portion near one end which contains a 
glass ball. Below this expansion it is graduated in tenths to one, 
and above the expanded portion to loi (Fig. 30). To one end 
of this tube is attached a piece of rubber tube which has a bone 
nipple at its other extremity. 

The pipet for the estimation of the white cells differs only in 
that it is larger and is graduated in tenths to one, and then above 
the expanded portion to 11. It will be readily seen that after 
the pipet for the red cells be filled with blood to i, and then the 
solution be added until it reaches loi, the diluting of the blood 
w^ill be one part of blood in 99 parts of the diluent, since there 
are 100 parts of solution between i and loi (see Method of Fill- 
ing Tubes, Fig. 31). The rubber tubing is now removed and the 



COUNTING OF THE BLOOD-CORPUSCLES. 



53 



one part in the graduated portion is blown out. I usually fill 
the tube with blood to 0.5 and add the solution to loi, which 
minus the i below the expansion gives a dilution of i in 200. 




0100mm j^^M 






Fig. 30.— Thoma-Zeiss hemocytometer : a. Slide used in counting ; b, sectional view ; 
c, portion of ruled bottom of well ; d, red pipet ; <?, white pipet. 

The white pipet when filled to i with blood and the solution 
added to reach 1 1 gives us a dilution of i part of blood in 9 parts 
of the diluent, after forcing out the liquid in the capillary tube 




Fig. 31. — Method of collecting blood into the graduated pipet. 

below I. Here again I prefer to fill the tube with blood to the 
0.5 graduation, and with the solution to 11, a dilution of i part 



54 THE BLOOD. 

in 20. The diluting fluids should be carefully watched lest they 
become cloudy or contain any sediment which may obstruct the 
lumen of the capillary tube. To the summit of the drop of blood 
collected from either the ear or the finger the tip of the pipet is 
touched and gentle suction apphed to the rubber tube, the nipple 
of which is placed between the lips (Fig. 31). 

When the blood is drawn to the desired graduation, the tongue 
is placed against the opening of the nipple and the tube withdrawn 
from the drop, its tip cleansed with a soft towel, and the end of 
the tube now immersed in the diluting fluid. Suction is again 
made, and the pipet rotated rapidly between the thumb and index- 
finger as the diluting fluid enters (always holding the pipet in the 
vertical position). The glass ball in the expanded portion facili- 
tates in effecting a dissemination of the blood throughout the 
diluting fluid; and when sufficient of the solution has been added 
to reach the loi graduation, the tongue is again placed over the 
opening of the nipple, and the tube withdrawn from the solution. 
The rubber tube should be removed from the pipet, and the 
diluting fluid occupying the tube below its expanded portion 
should be blown out, since it plays no part in the dilution. 

Caution. — In case the tube be held horizontally while filling 
it with the diluent, the solution is liable to creep along the side of 
the tube and pass the loi graduation before the expanded portion 
is entirely filled, thereby greatly increasing the dilution and ren- 
dering worthless the results. Unless the rotation of the tube be 
rapid during its filhng, the blood is hable to coagulate in the ex- 
panded portion or to be unequally distributed, when again the 
result obtained is of little value. Should suction be applied too 
vigorously, the liquid may be drawn along the side of the tube to 
beyond loi before the expanded portion is fifled. 

If not avoided, these errors are responsible for more mistakes 
than any other steps in the estimation of either the red or 
the white corpuscles. After the tubes have been filled they may 
be placed together and secured by a rubber band. Unless the 
ends of the capillary tubes are permitted to touch some object, 
they will remain in perfect condition for hours, and further 
progress in the technic need not be continued immediately. 

Counting. — Next in the process for the estimation of the 
blood-cells we have to consider the slide, which contains at its 
center a chamber divided into 400 squares, each of these squares 
being -^ of a mm. square and yq- of a mm. deep, and having a 
capacity of tV^^to >^ To^TTo'o ^^ 2. mm. (Fig. 32). This cham- 
ber is surrounded by a narrow channel. Every sixteen of 
these small squares are surrounded by a double row of Hues, and 
are known as a great square (Fig. 32, left corner). 



COUNTING OF THE BLOOD-CORPUSCLES. 



55 



There is a special ground cover-glass which must be brought in 
direct apposition with the shde in order that each of the squares be 
exactly tq oi a. mm. in depth. The tube containing the diluted 
blood is rotated rapidly between the thumb and finger. From four 
to eight drops of blood are forced out of the pipet by blowing 
through the rubber tube. A single drop is made to collect at the 
tip of the pipet and transferred to the center of the slide. Place 
the special cover-glass upon the edge of the raised portion of the 



















6^ 


(-1 


0°°! 


@ 






^~N 










6 


,5^. 


oo 

K°9 


(i) 


n 


f 


¥ 




(^ 




) oc 


o H.1 


@ 




i> 


/ 


'•>->' ^ -^ 




Zi> 


----^.-r'-*' 




/ ^^ " 


— -, 








~~ - 













































































































































Fig. 32.— Thoma-Zeiss counting chamber. Capacity, jj;. mm. Sixteen great sauares 
heavily outlined within the cross-lines, and bounded by double lines. Each^ great ^sXre 

^^f^lfrlA~J{\f' !r- P™J^cted to upper left corner is one great square showing arrange- 
WH I ^^\ ^"'^ number in each small square ; also leukocytes in last colunTn Ri4t 

hand shows small square containing 11 red cells. cummn. Ki^nt 

The floor of the chamber is ruled into 400 small squares. 

shde. The forefingers are placed upon the cover-glass, while the 
second fingers and thumbs hold the slide at its corners. The fore- 
fingers are forced forward, using marked pressure until the cover- 
glass has passed beyond the opposite margin of the channel which 
surrounds the graduated chamber. 



56 THE BLOOD. 

Should the cover-glass be in direct apposition with the glass 
shelf surrounding the chamber, there will be displayed at different 
points the colors of the rainbow {Newton's rings). Considerable 
skill is required in the application of the cover-glass. It may be 
permitted to drop gently upon the chamber, and should Newton's 
rings not appear, gentle pressure may be made with a needle, 
when they are hkely to be seen; but should they disappear when 
the pressure is removed, it is evident that some dirt rests between 
the shelf and the cover-glass. 

After the cover-glass has been successfully apphed, the slide 
is placed upon the microscope, and should first be brought under 
the focus of a two-thirds objective, using a No. i or 2 eye-piece. 
If the corpuscles appear equally distributed throughout the field, 
a one-fifth or one-sixth objective is brought into focus. Either 
of these objectives will be found to include 16 of the small squares 
(one great square) (Fig. 32). In the counting of the red cells 
it is necessary to count the cells in five great squares (80 small 
squares). Since the factor to be employed in our estimation is 
extremely large, strict rules as to counting are necessary. Con- 
sidering only the 16 squares surrounded by the double fines (Fig. 
32), count the number of cells in each column of four squares. 

Directions for Counting Red Cells. — In this estimation all 
corpuscles touching upon the top and left-hand boundary lines 
are included in the square, while those resting upon the right 
and bottom lines are to be included in the count of the contiguous 
squares (see Fig. 32, number of cells in each square and in 
column of squares being given). In this way it will be found 
easy to count the cells in the left-hand column and passing to 
the adjacent right-hand column until the four columns have been 
counted, which will give the total blood-cells for one great square 
(16 small squares). The sHde is now moved and four other 
great squares are counted in like manner. A mechanical stage 
greatly facilitates this process, yet it is not absolutely necessary. 

Having found the number of cells in five great squares, we 
return to the degree of our dilution and the capacity of the small 
square as the other factors for the estimation of the number of 
red cells per cubic millimeter. Suppose our dilution to have been 
I in 200, and the number of red cells found in five great squares 
(80 small squares), 87, 95, 93, 86, 89 respectively, a total of 450. 
Factors employed are: 

450 = no. of cells, 

^^■g- mm. == area small square. 
Y^o mm. = depth of small square. 



^00 



dilution. 



80 = number small squares counted. 



COUNTING OF THE BLOOD-CORPUSCLES. 57 

Hence 450 X 400 X 10 X 200 = 360,000,000 ~ So = 4,500,- 
000, the number of cells in i c.mm. of undiluted blood. A rapid 
method for arriving at the number of cells per cubic millimeter of 
undiluted blood (dilution 1-200) is to add four ciphers to the 
number of cells found in 80 small squares, 450, which gives us 
4,500,000. 

Leukocyte Count. — The counting of the white cells differs 
only in that we are dealing with a much lower dilution of the blood, 
and that we count 400 instead of 80 small squares. The 400 
small squares may often be brought into the field under a two- 
thirds lens, and when the number of leukocytes is not at all great, 
they may be readily counted. When the number of leukocytes 
is high, it is necessary to use a one-fifth lens, starting at the upper 
left-hand corner of the slide, and moving the slide gently so as 
to move each column of great squares until the entire slide has 
been covered (Fig. 32). Here again the same precaution of 
counting all cells touching upon the top and left-hand Hnes, and 
of omitting those cells resting upon the right and bottom lines, 
must be observed. 

After counting the cells in 400 small squares, dilution 1-20, 
see other factors for estimating the red cells. The direct method 
for estimating the number of leukocytes in i c.mm. of undiluted 
blood is to multiply the number of cells found in the 400 squares 
by 200. Suppose the number found to be 35, and the dilution 
I in 20: 35 X 200 = 7000. I have not been able to obtain satis- 
factory results by using the pipet devised for the estimation of the 
red cells. 

Care of the Hemocytometer. — Equally important with other 
steps in the counting of the blood-cells is the cleaning of the pipet, 
which should be done immediately after the count is made. 

Remove the rubber tube and place it upon the graduated end 
of the pipet. Force out the contents and fill with distilled water. 
Rotate rapidly between the thumb and finger, and again expel 
the water. Repeat this process three or four times; remove the 
rubber tube and place it upon the end of the pipet to which it 
belongs; fill the pipet with distilled water, and following the 
expulsion of this liquid the pipet is dried by blowing through it. 

If this method be conducted carefully, there is no need for 
further cleansing of the instrument. Many prefer to use ether as 
the last solution placed in the tube, but I have found better results 
to follow the employment of distilled Avater. The counting 
chamber is to be cleansed with water only, and rubbed with a 
camel's-hair brush. 

Caution. — Blood allowed to dry in the pipet is dislodged with 



58 THE BLOOD. 

great difficulty; and in case the pipet for the white cells becomes 
darkened, this color is removed by filling the pipet with acid. A 
particle of blood obstructing the lumen of the pipet may be removed 
by inserting a bristle into the pipet and then attempting suction. 
The graduated slide is cleansed in distilled water, care being 
taken to avoid friction, since the fine rulings are easily destroyed. 
Blood may be kept in the pipet for twenty-four hours, and if they 
are thoroughly rotated before expelling any of their contents, the 
cells will be found equally disseminated throughout the mixture. 
This avoids the necessity of carrying a microscope to the bedside, 
and brings hematologic study within the domain of general 
medicine. 

Oliver's Hemocytometer. — With Ohver's hemocytometer 
(Fig. 33) the estimating of the corpuscles depends upon an optic 
effect without directly counting them, and for all practical work the 
actual counting of the cells may be avoided by the use of this 
instrument, unless there be present a high degree of leukocytosis. 
The principle of this instrument is based upon the fact that a 
quantity of blood diluted with Hayem's solution is placed in a 
test-tube the sides of which are flattened so that the mouth forms 
a right angle of about 15 by 5 mm. A candle- flame is looked 
at through the mixture, and when a certain degree of dilution is 
reached, a bright horizontal line appears on the glass. This line 
is the result of a number of minute images of the flame produced 
by the longitudinal striations of the glass, and in case the quantity 
and quality of the blood used are in every instance the same, the 
degree of opacity then depends upon the amount of Hayem's 
solution added. By noting this point one is able to estimate, with 
a fair degree of accuracy, the number of red corpuscles present 
in I c.mm. of undiluted blood. 

Method. — Collect the blood as previously described for estim- 
ating hemoglobin. Cleanse the pipet and bring its smaller extrem- 
ity in contact with the summit of the drop of blood, when it fills by 
capillary attraction. Wipe away all blood clinging to the outside 
of the tube. Fill a medicine dropper with Hayem's solution; im- 
mediately connect the dropper with the blunt end of the pipet (Fig. 
33), and wash the blood into the larger graduated tube. When the 
hemoglobin has been previously found to be 90 per cent, or more, it 
is usually justifiable to fill the large tube to the graduation 80; but 
should the hemoglobin be lower, the dilution should be correspond- 
ingly lessened. When the point is neared at which the flame image 
is Hkely to appear, the diluting fluid should be added in quantities 
of five to ten drops at a time, placing the thumb over the mouth 
of the tube and inverting it several times to effect a perfect mixture 



COUNTING OF THE BLOOD-CORPUSCLES. 



59 



of the blood and the additional solution. That portion of the 
solution which chngs to the surface of the thumb should be wiped 
upon the edge of the tube. When sufficient of Hayem's solution 




Fig- 33- — Oliver's hemocytometer : a, Measuring^ pipet ; b, dropper to contain Hayem's 
fluid ; c, mixing tube graduated in percentages ; rf, mode of making the observation (this 
must be done in a dark room) ; a, b, and c are natural size. 



has been added, the image suddenly becomes visible and it is 
seen more easily by rotating the tube upon its long axis. After 
the first detection of the image add Hayem's solution drop by 



6o THE BLOOD. 

drop until the horizontal line of the flame is visible across the 
short line of the tube. The appearance of the incomplete hne at 
the sides denotes the approaching reaction. This degree of 
opacity remains unchanged for several minutes. The whole 
process needs to be carried out in a dark room, shutting the diffused 
light of the candle from the eye as shown in figure 33, d. The tube 
should be held near the eye, and the operator stand at a distance 
of ten feet from the candle. Wax candles are preferable. 

ALKALINITY OF THE BLOOD. 

The alkalescence of the blood being due to the presence of 
carbonates,- bicarbonates, and albumins held in solution by the 
acid phosphates, it is difficult to estimate the changes in these 
several principles, and the variations in the reaction produced 
by the several processes in alkalimetry. When serum alone is 
used for the estimation (by titration), the alkahne principles of 
the clot are not included; and if laked blood is used, uncertain 
chemic changes are produced which depend upon the delicately 
balanced albumins and phosphates. It has been clearly shown 
that there exists in the blood — and in the serum — certain rather 
constant alkahne principles which are sufiiciently closely esti- 
mated by the processes about to be described as to render this 
knowledge of clinical value. Again, it is evident that the degree 
of difference between the alkalinity of normal and that of diseased 
blood displays rather wide variations. During life the reaction 
of the blood is alkahne owing to the presence of disodium phos- 
phate and sodium carbonate. The degree of alkalinity under 
normal conditions is estimated in terms of sodium hydrate, and 
corresponds to 182 to 218 mgm. for every 100 c.c. of blood. \^on 
Jaksch, however, makes a higher estimate of alkalinity — 260 
to 230 mgm.; while Canard places it at 203 to 276. 

Clinical Significance. — Decrease. — The alkalinity of the 
blood is low in women, children, and during the latter stage of 
digestion (when the hydrochloric acid and peptones are reabsorbed) 
and after violent exercise. Pathologically, a reduction occurs 
in severe anemias (primary or secondary), leukemia, pernicious 
anemia, chronic hepatic disease, nephritis, diabetes, pseudoleu- 
kemia, and in the cachexia resulting from cancer. High fever, 
general toxemia, the prolonged use of acids, and poisoning by 
acids or carbon monoxid are attended by a low alkahnity, as are 
also acute mania (stage of excitement) and epilepsy. In the 
latter it begins just prior to a seizure, and continues to fall after 
the convulsion, the reduction varying according to the muscular 



ALKALINITY OF THE BLOOD. 6 1 

contractions during tlie convulsion.* The normal alkalinity 
is restored five to six hours after a convulsion. 

Increase. — An increased alkahnity is to be found early during 
the process of digestion and after a cold bath. 

Kireewf in studying the blood of 25 cases of typhus fever found the alkalinity 
to increase with the advance of the disease, and to reach its maximum with the 
height of the disease. The alkalinity fell rapidly to normal in favorable cases. 
In three fatal cases the alkalinity remained above normal. 

Estimation of Alkalinity. — Lowy^s Method. — i. Place 45 
c.c. of a 0.25 per cent, solution of ammonium oxalate in a flask 
having a graduated neck. 

2. Collect 5 c.c. of venous blood from the arm into a syringe 
(see Bacteriology oj Blood) and immediately transfer it to the sodi- 
um solution, which prevents coagulation and dissolves the hemo- 
globin from the protoplasm of the erythrocytes. Titrate the 
mixture with a 0.04 per cent, solution of tartaric acid. Lacmoid 
paper that has been previously soaked in a concentrated solu- 
tion of magnesium sulphate serves as an indicator. The 
T^V normal solution contains 3 gm. to the liter, and i c.c. of 
this solution therefore corresponds to 0.0016 gm. of sodium 
hydrate; e. g., 10 c.c. of the ^V normal solution were required 
to neutralize 5 c.c. of blood — the alkahnity of this quantity 
of blood in terms of sodium hydrate is 0.016 gm. To deter- 
mine the alkahnity of 100 c.c. of blood, multiply 0.016 by 20 
(the portion of 100 c.c, yV being employed) which equals 0.32 gm. 

Reagents .—Normsl solution of tartaric acid (75 gm. to the liter). 

Lacmoid paper is prepared in the following manner: The 
mixture is made of 100 gm. of resorcin, 5 gm. of sodium nitrate, 
and 5 c.c. of distilled water, which when heated on an oil bath 
to a temperature of 110° C. gives a violet color. The flame is 
removed before this temperature is reached. Again heat to 115°- 
120° C. until the ammonium ceases to be evolved.. Dissolve 
the pure blue residue in water and precipitate with hydrochloric 
acid, cool, filter with the aid of a suction pump, and wash with 
a small quantity of water. Again dissolve in absolute alcohol, 
filter, and evaporate in an ammonia-free atmosphere. This 
pigmerbt crystallizes in reddish-brown glistening plates; one gm. 
of which is dissolved in 1000 c.c. of 45 per cent, alcohol. Im- 
merse narrow strips of Swedish filter-paper in this solution for 
several minutes, dry them in the air, and place in a well- stoppered 
bottle. As this article is so seldom required, and as it necessitates 
such labor, it might be more advantageous for the student or 
practitioner to have this paper prepared by a chemist. 

Dare's Hemoalkalimeter. — Dare's instrument (Fig. 34) consists 
of a glass tube (a) provided with a glass stopper (b), and through 

* Pugh, "Jour. Mental Science," Jan., 1933, vol. xliv, p. 71. 
t "Medizinskoe Obosreni," l.xii, No. rg. 



62 



THE BLOOD. 




it passes an automatic capillary pipet which tapers at its exposed 
point. This capillary pipet has a capacity of 20 c.mm. (15 mgm. 
by weight) of blood. The stopper and the capillary pipet are 
fitted tightly into the tube (a), which is graduated to 3 c.c. to 
represent the equivalents in milHgrams of NaOH to 100 c.c. 
of blood. The upper end of the tube is expanded, and upon 
this expansion is a minute opening (c) for the admission of air. A 
medicine dropper graduated to 2 ex. and provided with a piece of 
rubber tubing which is applied to the exposed end of the capillary 
tube serves to introduce the test solution. The spectroscope is neces- 
sary, and Browning's pocket in- 
strument will be found satis- 
factory. 
t/iKiM/M am m ^ Test solution * 

Tartaric acid (Merck's 

reagent) o-o75 gn^* 

Alcohol (94 per cent.) 20 c.c. 

Distilled water q. s. 200 " 

Method oj Application. — ■ 
(i) Obtain a drop of blood from 
the tip of the finger; hold the 
tube horizontally and permit the 
exposed tip of the capillary pipet 
to touch the summit of a rather 
large drop of blood, when it fills 
by capillary attraction. (2) Hold 
the tube vertically and wash 
the contents of the pipet into 
the tube by forcing the distilled 
water from a medicine dropper 
through the pipet. This washing 
is continued until the distilled 
water, collected at the bottom of the tube, reaches the graduation 
zero (o). (3) Close the opening of the tube by the finger and 
invert the tube repeatedly until the blood and distilled water are 
thoroughly mixed. (4) A dropper is now filled with the acid 
reagent, and this solution is forced through the capillary pipet 
into the tube. 

Caution. — Cover the opening in the expanded portion of the 
large tube before releasing the pressure from the rubber bulb 
of the dropper. (5) Without detaching the dropper, hold it 
in a vertical position and invert the tube several times. (6) 
Place that portion of tube (a) below the graduation (6) in the 



Fig. 34. — Dare's hemoalkalimeter. 



ALKALINITY OF THE BLOOD. 63 

cleft of the spectroscope, and examine for the existence of the 
absorption-bands of oxyhemoglobin (see Spectra, Fig. 24, page 
44). The acid solution should be added carefully after each 
examination until these bands disappear. The bands will be 
noticed to fade gradually as the point of neutrahzation is ap- 
proached. Invert the tube (a) after each additional drop of the 
acid solution. 

Upon the disappearance of the bands of oxyhemoglobin the 
test is completed. Note the result from the scale on the tube 
(a), which is graduated in both cubic centimeters and the equiva- 
lents expressed in milhgrams of sodium hydrate to 100 c.c. of 
blood. 



SCALE OF EQUIVALENTS COMPUTED FROM A BASIS OF 15 MGM. 
OF BLOOD TO 2 C.C. OF ACID SOLUTION. ONE TWO- 
HUNDREDTHS OF THE NORMAL. 

Cubic Centimeters Milligrams of NaOH to loo 

of Reagent. Cubic Centimeters of Blood. 



6 345-0 

4 - 319-0 

2 292.0 

o 266.0 

8 239.0 

6 212.0 

4 176.0 

2 169.0 

o ^i3-o 

8 96.0 

6 79-0 

4 SZ-'^ 

2 26.6 



TT C TT O 

"The equivalent weight of tartaric acid ^ ^ ^ " = 149.64. 

Tartaric acid being dibasic, one-half the number of molecules 
are taken to make a normal solution which equals 75 gm. (ap- 
proximately) to a liter; for the present solution there is taken 
-^-^ of the normal, which is equivalent to 375 mgm. to a Hter. 
Sodium hydrate has 40 atoms to its molecule, which gives an 
equivalent of 40 gm. to a Hter; therefore, -^\-^ of the normal 
tartaric acid solution will give an equivalent of 0.0002 mgm. of 
the alkali. Every 100 c.c. of blood will equal 266 mgm. of sodium 
hydrate" (Dare). 

For every 2.2 c.c. of reagent employed the equivalent of 292 
mgm. of sodium hydrate to 100 c.c. of blood is read from the 
graduation on tube (a). Dare employed open gashght in his 
observations. 



64 THE BLOOD. 



ACIDITY OF THE BLOOD. 

Certain of the salts in the blood are not saturated; e. g.y 
NaHCOg and NaH2P04. It is noteworthy that these give an 
alkaline reaction to litmus, but an acid reaction to phenolphthalein, 
and are capable of combining with bases. Fresh blood is alkaline, 
while serum causes an acid reaction with phenolphthalein. The 
basic capacity of the blood is the power its salts possess to neutrahze 
bases. Kraus has estimated the basic capacity of normal venous 
blood at 0.162 to 0.232 per cent. NaOH.* 

Clinical Significance. — ^x\n increase has been observed in 
fevers of from 0.209 to 0.272 per cent. NaOH ; and to reach 0.347 
per cent, in diabetes (Kraus j. 



COMPOSITION OF THE WHOLE BLOOD. 

Albumins. — The albuminous principles in the normal blood 
as found in the circulation are hemoglobin, serum-albumin, serum- 
globulin, and fibrinogen. Shed blood contains a nucleoproteid 
principle derived from the nuclei of leukocytes or from the red 
cells; and this substance combines with the calcium salts to form 
fibrin ferment ("prothrombi"). In certain diseased conditions 
(e. g., brain abscess) a small quantity of albumose has been found. 
The entire proteid group of the blood has been estimated by von 
Jaksch at 22 per cent. ; Limbeck rates it at about 25 per cent., and 
Schmidt records it from 10.82 to 16.63 P^^ cent. 

Clinical Significance. — A relative increase of albumin is oc- 
casioned by marked loss of fluids; e. g., in cholera and diarrhea; 
also in acute articular rheumatism, pleurisy, pneumonia, ery- 
sipelas, and other acute inflammatory processes. 

Reduction of the total albumin may accompany infectious 
diseases with high fever, even though the number of red cells 
remains normal; and early in chronic nephritis, in pernicious 
anemia, malaria, leukemia, pyemia, and in secondary anemia. 

Peptone. — Peptone, a constituent of cadaveric blood, does 
not appear to have been satisfactorily demonstrated in the circu- 
lating blood. However, when blood is allowed to stand for several 
hours, a reaction for peptones may be obtained. Albumose 
has been found in leukemic blood when the eosinophilic cells 
were numerous. We may here allude to the great similarity 
of the reactions caused by the albumose and those produced by 
globin (see Albumosuria, page 216). Quantitative estimation of 
the total albumin of the blood has not been considered, and the 

* '"Zeit. f. Heilk.," vol. x, p. 106; also "Arch. f. exper. Path.," vol. xxvi. 



COMPOSITION OF THE WHOLE BLOOD. 65 

reader is referred to special works on Chemical Physiology and 
Pathology for specific knowledge upon this subject. 

Inorganic Substances of the Blood. — Here again the subject 
falls outside the scope of this chapter. The estimation of the 
quantity of the blood ash has been briefly described, but for other 
and complete description the reader is referred to special works 
on Physiology and Pathology. 

Urea. — Traces of urea are normally to be found in the blood, 
0.016 to 0.02 per cent. (Simon), and an increase is observed 
in fevers, cholera asiatica, cholera infantum, eclampsia, and also 
in renal conditions when it is imperfectly eliminated by the kidneys. 
For determination and the detection of urea in the blood see 
Urine (Hoppe-Seyler's method). 

Uric Acid. — Traces of uric acid are demonstrable in normal 
blood. An increase has been observed in appreciable amounts, 
varying greatly with the type of disease present, during the course 
of pneumonia, anemia, cardiac embarrassment, acute gout, leu- 
kemia, nephritis (88.88 per cent, of cases, v. Jaksch). It has 
been shown that an increased elimination of the uric acid through 
the urine is accompHshed by an increased quantity of uric acid 
in the blood, but this condition is not constant. Lowered al- 
kalinity of the blood in the infectious fevers stands as an excep- 
tion to this rule. 

Method of Detection. — Obtain loo c.c. of blood (see page 34) 
and immediately transfer to a beaker. Dilute with three or four 
times its own volume of distilled water, and heat on a water-bath. 
When coagulation begins, a 0.5 per cent, solution of acetic acid 
is added in small quantities until a faint acid reaction is given. 
Continue the heat for twenty minutes, when the albumin will be 
found precipitated as brownish particles. Filter hot, heat, and 
wash the precipitate with hot water. Again add small quantities 
of acetic acid solution and bring both filtrate and washing to the 
boihng-point. Decant, filter, add a small quantity of disodic 
phosphate, and continue according to Ludwig-Salkowski's method 
(see page 198). Treat the first filtrate with hydrochloric acid and 
evaporate to about 10 c.c. Allow to stand for twenty-four hours 
and separate the precipitated uric acid by filtering, and continue 
examination of the filtrate for uric acid (see Urine). The murexid 
test (see page 196) may be apphed directly to the fluid before the 
uric acid has had time to precipitate; and its employment is 
necessary when no uric acid separates from the solution after 
standing for twenty-four hours. 

Glycogen. — Blood smeared upon slides or cover-glasses 
in the usual manner and dried in the air is stained for from three 



66 THE BLOOD. 

to five minutes with the following: lodin, pure, i part, potassium 
iodid 3 parts, water loo parts, pulverized acacia in excess. In 
the presence of glycogen there are a number of small granules 
of a mahogany-brown tint in the leukocytes and occasionally 
in the plasma. Question has arisen as to whether or not these 
granules represent subjects more closely alHed to amyloid than 
to glycogen. The extracellular granules are both fine and coarse, 
varying from |^ /-< in diameter, and appear to be the only form 
found in the normal blood. An increase in the number of gran- 
ules as seen in disease is shown by intracellular granules. Extra- 
cellular granules are possibly derived through degeneration of 
leukocytes. Neutrophilic leukocytes have been known to 
contain these granules in case of leukemia and diabetes, and 
they have been found in the plasma in connection with pathologic 
conditions. After a review of the current literature on this subject 
it is evident that further observations are needed to establish 
any valuable chnical data. 

Fat (Lipemia) and Fatty Acids. — Normal blood contains 
between 0.75 and 0.85 per cent, of fats.* Particles of fat may be 
demonstrated in the blood by fixing the films in a one per cent, 
solution of osmic acid for twenty-four hours, and staining from 
one-half to one minute with a one-half of one per cent, aqueous 
solution of eosin. The particles of fat having stained black 
with the osmic acid, the remainder of the field takes the eosin 
stain (Fig. 35). In view of the fact that all granules staining black 
may not be fat a control preparation is necessary, and should be con- 
ducted as follows: Fix the film twenty- four hours in alcohol and 
ether, and then in the osmic acid for twenty- four hours; counter- 
stain with eosin, extract the fat by ether, and the absence of black 
particles in the cells and plasma is evidence that the blackening 
displayed by the former specimen was due to fat. Free fat 
(palmitin, stearin, and olein) may be detected in the blood in 
health and in disease, but it is usually present in comparatively 
small amounts, and while recognized wath some difficulty under 
an oil-immersion objective, the granules are at times conspicuous. 

Quantitative Estimation. — Collect from 5 to 10 gm. of 
blood and dilute with 100 to 200 gm. of 96 per cent, alcohol ; 
mix thoroughly, allow to stand for twenty-four to forty-eight 
hours, and filter. Subject the deposit collected on the filter to 
a repetition of the above treatment. The part remaining is treated 
with ether, and the remainder digested and thoroughly shaken 
with ether. Collect the various alcoholic and ethereal extracts, 
evaporate slowly to dryness, extract with absolute ether, dry, and 

* Bonninger, "Zeit. f. klin. Med.," igoo, vol. xli, pts. i and 2. 



COMPOSITION OF THE WHOLE BLOOD. 67 

weigh (Hoppe-Seyler). Extract filter-paper to recover any fat 
it may have withheld (see special works on physiologic chemistry). 
Clinical Significance. — The quantity of fat in the blood is 
increased after a heavy meal and in acute alcoholism. An excess 
of 0.05 to 0.16 per cent, has been found in the blood of diabetes, 
0.1 to 0.5 per cent, in nephritis, 0.15 per cent, in pneumonia, 
and 0.16 per cent, in typhoid fever. An increased quantity has 
been observed in starvation, phthisis, fatty embolism, carcinoma 
of esophagus, and poisoning by carbonic oxid. A fat-splitting 
ferment has been detected in the blood.* V. Jaksch has demon- 







Fig- 35> — Blood from a case of lipemia, stained with osmic acid : upper half of field 
cleared with oil of turpentine; lower half shows the fat-droplets and granules stained with 
osmic acid between the blood-corpuscles; enlargement, loo diameters (Gumprecht), 

strated fatty acids in the blood of diabetic coma, acute yellow 
atrophy (hepatic), acute infections, and leukemia. 

Glucose. — Normal blood contains a trace of glucose, and this 
quantity may fluctuate, depending upon a diet rich in carbohy- 
drates (increase) or by muscular exercise and hunger (decrease). 
It has been found in the blood of health by Limbeck five hours 
after a meal (0.075 to 0.089 P^^ cent.). Freund and Trinkler 
found glucose increased in the blood from cases of cancer, and 
were able to reduce cupric oxid when exempt from albumins. 
Trinkler found 3 per cent, of glucose in the blood of carcinoma. 

* Hanroit, "Compt. Rend. Soc. Biol.," 1896, p. 925. 



68 THE BLOOD. 

Depending upon the character and stage of the disease, glucose 
has been found to reach 0.9 per cent, in the blood of diabetes.* 

Estimation of Glucose in the Blood. — A quantity of blood 
is weighed, freed from albumin by boiling with an equal quantity 
of sodium sulphate, and then filtered; the precipitate is washed 
carefully, and the filtrate treated with Fehling's solution. A 
more positive demonstration is by polarimetry (see page 236). The 
blood should be fresh, lest the glycolytic ferment produce mis- 
leading reactions. It is not known upon what the glycolytic 
principle of normal blood depends. 

Diabetic Blood. — A test for diabetic blood worthy of descrip- 
tion is Williamson's. Knowledge obtained from any special 
reaction of the blood is impracticable unless it enables us to 
recognize diabetes at an earlier period than can be done by 
urinalysis; and the majority of writers on this subject hold that 
this has not been proved. Diabetic blood is rich in fats. 

Williamson's test is easy of execution, and consists in the 
decolorizing of an aqueous solution of methylene-blue. Col- 
lect two drops (20 c.mm.) of blood, and dissolve in 40 c.mm. of 
water; then add i c.c. of methylene-blue solution (1-6000) and 
40 c.mm. of Hquor potassae (specific gravity 1.058). Place the 
vessel containing the mixture in boiling water for four minutes. 
The solution is decolorized with diabetic blood, and remains 
a deep blue with normal blood. 

Clinical Significance. — Williamson has been unable to obtain 
this reaction with the blood from other forms of disease. The 
reaction is produced by diabetic urine. Wllhamson obtained 
positive reaction in nine cases of diabetes, and negative results in 
130 non-diabetic cases. Adler confirmed the vahdity of Wilham- 
son's reaction, and attributes it to reduced alkahnity of the blood. 
He has also shown that Bremer's test for diabetes is not of diag- 
nostic value. 

Red Cells. — Sugar in the blood extracts water from the tissues 
into the vessels, thus diluting the blood; but blood concentration 
is soon accomphshed owing to the increased diuresis. It is the 
influence of these processes that is responsible for the wide varia- 
tion in the number of cells found per cubic millimeter, and on this 
account it is impossible to arrive at any constant number of ery- 
throcytes for this disease. Even during the period of cachexia 
and anemia in diabetes blood concentrations may be found well 
marked, and the number of red cells high. The hemoglobin 
may fluctuate between wide limitations and is doubtless depen- 
dent upon similar conditions. 

* Hoppe-Seyler, "Physiological Chemistry," 1881. 



COMPOSITION OF THE WHOLE BLOOD. 69 

Leukocytes. — The number of leukocytes varies greatly in 
different cases and at dift'erent times during the course of the same 
case; yet leukocytosis has not in my experience been a common 
occurrence, though the leukocytes have been seen to reach 10,000 to 
1 2,000 per cubic millimeter. Cabot did not observe leukocytosis in 
the study of thirteen cases, and during diabetic coma he found the 
leukocytes to number 4200 per cubic millimeter, while in another, 
a child of eight years, there were 49,000 leukocytes present. 

Acetonemia. — It has been found by Deichmiiller and by 
V. Jaksch that by extracting the blood with ether and by distilla- 
tion a principle could be isolated which gives a reaction for acetone. 
This principle was found to be increased in fevers. 

Cholemia. — This term has been apphed to the presence of 
bihary acids in the blood, yet such bloods commonly contain 
cholesterin. 

Icteric blood appears to the naked eye as yellowish in color, 
and in its serum or foam may be seen small particles of bile-pig- 
ment. The apphcation of heat (70° to 80° C.) causes the red 
bihrubin to be replaced by a greenish tinge — bihverdin. Lim- 
beck's analyses of icteric blood show an increase of nitrogens 
from 3.29 to 3.52 per cent., while the chlorids were diminished 
both in the blood and in the serum. An increase in the volume 
of red cells is mentioned. 

Isotonic Tension. — Low isotonic tension and increased 
resistance of the red cells are peculiar to jaundice (see page 74). 
The effect exercised by the bile acids upon the hemoglobin prob- 
ably renders it more freely soluble. Bihrubin may be demon- 
strated in the blood when urobihn exists in the urine. 

Method. — Collect the blood either by a hypodermic syringe 
from the vein or by a wet cup, place in a bowl, allow to coagulate, 
and after two or more hours decant serum and filter. The 
filtrate displays a yellow tint when bilirubin is present, and be- 
comes green after heating for several hours at 35° C. A mere 
trace of bile-pigment is detected in this manner. 

Biliary Acids in the Serum. — Pettenkofer's Method. — 
Remove the albumins by boihng or by alcohol; filter and treat 
the filtrate with lead acetate and with ammonia. The acids are 
precipitated with lead compounds. Wash the precipitate on a 
filter, boil in alcohol, filter, and decompose the lead salt by car- 
bonate of soda. Again filter, and evaporate to dryness. The 
acids are extracted by boihng in absolute alcohol. Evaporate 
the alcohoHc extract when bihary acids crystallize, and an amor- 
phous substance remains from which crystals are obtained after 
extracting with ether (see works on physiological chemistry) . 



70 THE BLOOD. 

Globulicidal Properties of Serum. — Serum of pathologic 
blood when brought in contact with normal blood often causes 
the red cells to dissolve and the hemoglobin to be replaced by a 
greenish hue. Spectroscopic examination reveals the presence 
of hematoidin instead of hemoglobin in such mixtures. Globu- 
Hcidal properties may be well marked in the serum of the 
primary anemias, purpura, malaria, leukemia, erysipelas, typhoid 
fever, pneumonia, and nephritis. Buchner has shown that the 
globuhcidal activity is more marked in serum poor in salts, and 
that it is also diminished after the addition of salts. A close 
relation must exist between the globuhcidal property of the serum. 
The blood of one animal brought in contact with the blood of 
another animal displays coagulative power, which may be greatly 
lessened by the addition of salt or by heating to 50° C. ; yet these 
do not totally destroy any toxicity that may exist in the serum. 
Toxicity of the serum depends principally upon certain retained 
albuminoid bodies. Wide variations in the toxicity, globuhcidal 
and coagulative properties of different serums may be found in 
both health and disease (see Serum-diagnosis, page 116). 

Diastatic Ferment of Blood. — The power of the blood in 
both health and in disease to digest starch has recently received 
cHnical attention. To demonstrate this property add i c.c. of 
blood to 50 c.c. of starch solution, stand several hours in an in- 
cubator, and test for glucose with Fehling's solution. Two 
c.c. of normal human blood when added to 50 c.c. of starch solu- 
tion and kept at a temperature of 30° C. for twenty-four hours 
was found by Castellino and Pracca to yield 0.07 per cent, of 
sugar. Diastatic fermentation is most active in arterial blood 
that is kept at a temperature of 30° to 38° C, and inhibition is 
observed at 75° C. (Cavazzani). 

Clinical Significance. — The fermentative power of the blood 
is increased in chlorosis, leukemia, nephritis, pneumonia, malaria, 
hepatic cirrhosis, and carcinoma, and was found decreased in 
other forms of disease.* The addition of nuclein inhibits the 
diastatic ferment, while sodium sulphate and sodium chlorid 
intensify it. 

CRYOSCOPY OF THE BLOOD. 

Cryoscopy as applied to the body fluids and secretions, espe- 
cially to the blood, has, as yet, yielded but few definite results. 
Waldvogel's descriptionf of the technic for determining the 
freezing-point of fluids is in brief as follows: Pour 8 to 10 c.c. 

* Cavazzani and Pracca, "Arch. p. 1. sci. med.," vol. xvii, No. 6. 
t "Arch. f. exper. Path.," vol. xlvi, i and 2. 



CRYOSCOPY OF THE BLOOD. 



71 



of the blood or urine into a small test-tube, around the top of 
which a rubber ring has been placed. This tube fits into a larger 
one with a space of about one centimeter between the bottoms of 
the tubes, and of 2 or 3 mm. between the walls. Both are then 
placed together in the freezing (ice and salt) mixture (Fig. 36). 
The temperature is determined by a small thermometer, graduated 
in fiftieths or hundredths of a degree C. to four degrees below 




Cryoscopic apparatus. 



the freezing-point, which is inserted in the blood or the urine. 
The thermometer is surrounded by a rubber ring which prevents 
it touching either the bottom or the wall of the tube. When 
it registers —0.52° C, the fluid is stirred with the thermometer, 
and it congeals almost instantly into a sohd mass of ice. 

Diluting the fluid a little does not interfere with the deter- 
mination of the freezing-point. Blood must be placed on ice or 



72 THE BLOOD. 

in a refrigerator for forty-eight hours before it is tested. The 
zero must correspond to the freezing-point of distilled water as 
verified from time to time. For method of obtaining blood for 
cryoscopic study, see Bacteriology of Blood. 

The molecular concentration of any liquid is expressed in 
its freezing-point, which lowers proportionately to the degree 
of concentration. Osmosis, too, has an important bearing on 
this phenomenon, since the osmotic pressure between fluids 
separated by a membrane is directly proportional to the mole- 
cules held in suspension; thus the freezing-point of a solution 
containing several substances is lowered to the equivalent of the 
sums of the freezing-points of each substance suspended in the 
Hquid. Human blood under normal physiologic conditions dis- 
plays a fixed freezing-point — 0.56° C. — below distilled water 
(Kummel). 

Clinical Significance. — When the metabohc products are 
retained in the blood as a result of renal insufficiency, its molec- 
ular concentration is increased and consequently its freezing- 
point lowered, as has been found in the blood of nephritis, hydro- 
nephrosis, pyonephrosis; and experimentally in animals after 
ligation of the ureters. The freezing-point of the blood is un- 
changed when the remaining kidney compensates after the re- 
moval of its fellow. 

When the freezing-point of the blood is lowered to — 0.58° to 
— 0.61° C. , both kidneys are diseased, and surgical operation of 
any kind should be interdicted until the freezing-point is about 
— 0.56° C. A freezing-point of the urine less than — 0.9° C. indi- 
cates kidney insufficiency, and whenever one kidney is supposed to 
be affected, the freezing-point of the urine obtained by catheteriza- 
tion of the ureters or by segregation may be of chnical value. 
Urine from the diseased kidney will congeal at a higher point than 
will that from its fellow; e. g., urine from the diseased kidney 
freezes at — 0.50° C, and urine from a healthy kidney at — 1.75° 
C. Generally speaking, it is impossible to draw definite deduc- 
tions from the estimation of the freezing-point of the urine, owing 
to the wide physiologic limits between which it may fluctuate — 
from — 0.1° to — 2.0° C. under normal conditions.* Tinker 
has recently averred the value of cryoscopy as an index to renal 
insufficiency.f The method of Claude and Balthazard has 
recently appeared in a detailed translation by F. Burthe.t Thus 
far the methods of cryoscopy are given for physiologists' use 
only, and are not readily adapted to clinical use. 

* Kummel, " Verhandlungen der deutsch. Gesellsch. f. Chir.," 29th Congress. 
t "Johns Hopkins Hosp. Bui.," June, 1903, p. 162. 
J "Med. News," Jan. 23, 1904, p. 149. 



OSMOTIC PROPERTIES OF THE BLOOD. 75 



OSMOTIC PROPERTIES OF THE BLOOD. 

The red cells will be found to dissolve promptly when a drop 
of blood is placed in distilled water, but placed in a solution of 
salt, of sufficient concentration, the red cells retain their hemo- 
globin, and are precipitated at the bottom of the Hquid. This 
solution of the red cells is the result of the law of osmosis: i. e.y 
when two solutions of different concentrations are separated by 
an animal membrane, these solutions pass through the membrane 
until they are of equal densities, or the quantity of salt in each 
is equal. The force producing this interchange is termed " osmotic 
tension"; and the two Hquids containing an equal quantity 
of salt are termed "isotonic." Fluids containing a greater or 
lesser quantity of diffusible salts than other solutions are termed 
" hyperisotonic " or "hypisotonic," and possess the faculty of 
extracting water from or yielding it to such fluids in accordance 
with the laws of osmosis. The red corpuscles in a normal speci- 
men of human blood are prevented from solution when added 
to a 0.46 per cent, solution of NaCl. We therefore regard the 
isotonic tension of human red corpuscles to be 0.46 per cent. 
NaCl. In this solution the red cells swell, absorb water, but 
do not give up their hemoglobin; and when placed in sufficiently 
strong solutions, the cells shrink, yielding water to the fluid. 

Normal Salt Solution. — A 0.9 per cent, solution of salt 
prevents either swelling or shrinking of the red cells. Therefore 
this strength solution represents the isotonic tension of the blood 
plasma, and is universally known as the normal salt solution. 

Lowering of the osmotic tension of the plasma of necessity 
leads first to swelling and eventually to solution of the red cells. 
The hyperisotonic property of the plasma is a physiologic safeguard 
for the preservation of the red cells after the introduction of large 
quantities of water into the circulation (hypodermoclysis). There 
may occur variations in osmotic tension which affect the volume 
of the red cells. Certain other diffusible principles, as albumins, 
also influence the isotonic relation of the blood; which shows that 
its isotonic properties do not depend entirely upon the presence 
of salt.- Limbeck found only 0.2 per cent, of salt in the red cells, 
while their isotonic tension equaled at least 0.46 per cent. NaCl. 
It has been further shown by Hamburger * that albumins, chlorids, 
and phosphates appear differently when under varying osmotic 
conditions. 

The addition of acid to blood causes phosphates and albumins 
to pass from the erythrocytes into the serum and the chlorids 

* "Arch. f. exper. Path.," vol. xii, p. 237. 



74 



THE BLOOD. 



change from the serum into the cells: the reverse phenomena 
follow the addition of an alkali. Probably most important among 
the functions of osmotic tension is the influence it exercises in 
causing the hemoglobin to be contained in the red cells. 

Clinical Significance. — Rather wide physiologic variations 
in the isotonic tension of the blood are to be observed normally; 
and that of the venous blood is regarded as being shghtly higher 
than is that of arterial blood. It is increased by the addition of 
hydrogen, nitrogen, arsenic, CO, COj, and acids; and is dimin- 
ished by a trace of alkalis or oxygen. During the course of 
typhoid fever, pneumonia, erysipelas, and other acute infections, 
the isotonic tension may be increased (Limbeck). It was also 
found increased in leukemia, secondary anemia, pregnancy, and 
lactation; but low in jaundice and in chlorosis. 



STUDY OF FIXED AND STAINED BLOOD, 
SLIDES AND COVER-GLASSES. 

The first step in the preparation of smears or films upon either 
cover-glasses or sHdes has been previously described on page 
35, and such spreads are fixed in one of the following manners: 

The method I have found 
most satisfactory and avail- 
able is the use of a strip of 
copper about J x 4 x 28 inches 
(Fig. 37), which is allowed to 
balance on a tripod, vv^ith the 
flame of a Bunsen burner be- 
neath one end of the copper. 
After the copper has been 
thoroughly heated, fiU a 
pipet with cold water and 
drop it on the copper at dif- 
ferent distances from the flame. At the point where the water 
boils, but is not excited into bubbles that bounce off the stage, 
place the cover-glasses or sHdes, specimen down, and allow them 
to heat for twenty minutes. They are then removed, labeled, and 
placed in small pasteboard boxes, where they may be kept for 
an indefinite time. 

Spreads may also be fixed by placing them in a Petri dish, 
specimen up, and this dish set within a larger dish containing a 
small quantity of 40 per cent, formahn. Cover the larger dish 
and permit the surface of the smears to be exposed to the fumes 




Fig- 37- — Stage for fixing blood. 



SLIDES AND COVER-GLASSES. 



75 



of the formalin for from twenty minutes to a few hours. Results 
from this method of fixation are, at times, unsatisfactory. 

Grasp a cover-glass or a shde containing a spread in the for- 
ceps and pass it rapidly through the flame of a Bunsen burner, 
care being taken that after each insertion into the flame the surface 
of the glass is touched upon the palmar surface of the hand. A 
guide to the degree of heat appHed is obtained in this way, and 
after four or five appHcations to the flame the specimen is often 




Fig. 38. — A convenient reagent stand for office work. 



well fixed; yet considerable skill is necessary for the successful 
employment of this method. 

Arrange the smears in a Petri dish, cover, and allow to stand 
in an incubator, at a temperature of 37° C, for twenty-four hours. 
A fixing solution containing — 

Osmic acid i gm. 

Sodium chlorid 0.6 " 

Distilled water 100 c.c. 

maybe applied at the time the films are made, (i) Wash a small 



76 THE BLOOD. 

camel's-hair brush in alcohol to remove all fats. (2) Immerse 
the brush in the fixing solution, and then touch it to the summit 
of the drop of blood, when the blood is disseminated through 
the brush, and is acted upon by the osmic-acid solution. (3) 
Smears are made by drawing the tip of the brush over the surface 
of a slide or cover-glass and are permitted to dry in the air.* 
A number of films may be made after a single apphcation of the 
brush to the blood. 

STAINING. 

The most essential points in the staining of blood are the 
results obtained by a given method and the simplicity of the 
method employed. In 1891 Romanowsky detailed a method for 
the staining of malarial parasites by which the chromatin and 
the cytoplasm were stained differently. Since the appearance of 
Romanowsky's original paper many have tried to perfect a similar 
staining method. Jenner detailed a most practical stain for 
blood; and Leishman simplified to some extent Jenner's method. 
It was not until 1902 that J. H. Wright gave to the profession a 
practical apphcation of this method. 

Eosin and Hematoxylin. — It has been my custom to employ 
this stain almost entirely in class work and rather extensively 
in my general clinical studies. The solutions necessary for this 
method of staining the blood are: first, one-half of one per cent, 
of eosin in 70 per cent, alcohol; and, second, Delafield's hema- 
toxylin : 

Hematoxylin crystals 4 gm. 

Alcohol (absolute) 25 c.c. 

Ammonia-alum crystals 52 gm. 

Distilled water 400 c.c. 

Glycerin 100 " 

Methyl-alcohol 100 " 

Preparation. — Place the alcohol in a mortar, add the hema- 
toxylin crystals, and rub until well dissolved ; then place in a clear 
glass bottle, cork loosely, and allow to stand exposed to the light 
for four days. Add the ammonia-alum crystals to the water 
and treat in a similar manner. At the end of four days mix these 
two solutions, shaking thoroughly, and after a few hours filter. 
The glycerin and methyl-alcohol are now added, and the mixture 
allowed to stand for several hours. The solution is now filtered, 
placed in a clear bottle, and allowed to stand exposed to the sun- 
light for six weeks (ripening process), when it will be found ready 
for use. 

* Kornilouitch, " Vratch/' Nov. 17, 1901, vol. xxii, No. 46. 



STAINING. 77 

Application of Stain. — First stain the specimen with the eosin 
for one-half minute; wash in water. Then, without drying, stain 
with hematoxylin for from one to three minutes, as the time varies 
greatly with different stains even though they be prepared in essen- 
tially the same manner. Wash and dry the specimen, and mount 
as before described. 

Instead of hematoxyhn, a two per cent, aqueous solution of 
methylene-blue may be employed for one-half minute. A mixture 
of eosin and hematoxylin has been suggested, but in my hands it 
gave unsatisfactory results ; a mixture of eosin and methylene-blue 
is serviceable for staining the malarial parasite. The eosin and 
hematoxyhn method possesses certain properties necessary for the 
study of the finer structure of the nuclei, karyokinetic figures, 
and basophihc granules, but is not generally conceded to be as 
valuable as Ehrhch's mixture for diagnostic purposes. In the 
greater part of clinical work, however, the former method, will 
be found to be most reliable and satisfactory. 

MICROSCOPIC EXAMINATION OF THE STAINED BLOOD. 

It is possible to determine the character of the specimen by 
a two-thirds or one-sixth objective, but in order to bring out 
clearly and to study in detail the morphology of the finer struct- 
ures of the cells and their granules a one-twelfth oil-immersion 
objective is required. 

Normal Blood. — Normal human blood when stained with 
eosin and hematoxylin displays certain characteristics which 
distinguish it quite clearly from the blood of animals (Plate 2), 
but disease is capable of producing retrograde changes, in which 
case the red cells, principally, are distorted and resemble those 
found in the lower forms of animal life; such changes depending 
entirely upon the variety and degree of disease present. Physio- 
logically, this condition is observed in blood from the umbilical 
cord of the fetus — an advantageous source from which to prepare 
spreads for class work, since nucleated red cells are present in 
considerable numbers (Plate 2). 

Fixing and Staining Combined. — Jenner's method for these 
two steps in hematologic technic deserves more than passing 
recognition. In the author's hands it has proved entirely satis- 
factory, and it has been further found that good results attend 
the use of this stain for specimens previously fixed by heat. Jen- 
ner's solution is apphed in the usual manner to an unfixed film, 
and permitted to stain for from one to three minutes; wash in 
water, ten to thirty seconds, until a pink tint appears. The red 



78 THE BLOOD. 

and white cells, nuclei, and granules are brought out clearly and 
definitely (Plate 7). The malarial parasite stains deeply (red), 
as a rule, but Jenner's method * cannot be said to equal that of 
eosin and hematoxyhn or of Nocht's method. f F. C. Wood J 
has reviewed the literature in reference to the various modifications 
of Jenner's method, and in addition suggests a rapid stain for the 
malarial parasite, the preparation of which stain can be found 
by reference to Wood's article. 

Jenner's Stain. — Place equal parts of an aqueous solution 
of yellow eosin (1.25 per cent.) and of an aqueous solution of 
medical methylene-blue (i per cent.) in a rather broad dish, mix 
thoroughly, cover, and allow to stand for twenty-four hours. 
Filter, and dry in an oven at 55° C. or in the air. The residue 
cKngs to the filter-paper, which is now to be pulverized and washed 
in distilled water. Shake well, and again wash upon a filter; 
dry, powder, and place in a bottle. Dissolve 0.5 gm. of powder 
in 100 c.c. of methyl-alcohol (Merck's alcohol for analytic use). 
G. Grubler's stains should be used. 

Wright's Method. — The blood when smeared on slides or 
cover-glasses is allowed to dry in the air. The spread blood does 
not stain well after it is exposed to the air for several months. 

1. Add to the specimen sufficient of an alcoholic solution of 
the stain to cover the film, and allow it to stand for one minute, 
to fix the corpuscles. 

2. To the alcoholic solution of the stain now on the specimen 
add water, drop by drop, until the stain becomes semitranslucent 
and a yellowish, metallic scum forms on the surface. Permit this 
diluted stain to cover the specimen for two or three minutes. 

3. Wash the hea\dly stained specimen in water until the film 
of blood gives a yellowish or pink tint to the naked eye. 

4. When the desired tint is reached, dry immediately between 
blotting-paper, lest decoloring be carried too far. The specimen 
is now ready to be mounted in Canada balsam. 

Microscopic Appearance of Stained Blood. — The red cells are 
orange or pink, and their nuclei are deep blue and their cytoplasm 
presents a bluish tint. Granular basic degeneration of the red 
cells is made evident by this stain. Polynuclear neutrophilic 
leukocytes show dark-blue or dark-lilac colored nuclei and the 
granules are of a reddish-lilac color. 

Lymphocytes have dark, purphsh-blue nuclei; the cytoplasm 
is robin's-egg blue, and in it are seen a few dark-blue or purphsh 
granules. 

* "Lancet," 1899, vol. i, p. 370. t "Ency. K. d. mik. Technik," p. 785. 

t "Med. News," A\ig. 8, 1903, p. 248. 



MICROSCOPIC EXAMINATION OF THE STAINED BLOOD. 79 

Eosinophils display blue or dark-lilac colored nuclei. The 
granules are stained red by the eosin (Plate 13), but the cytoplasm 
in which they are imbedded is of a blue color. 

Large mononuclears present blue or dark-lilac colored nuclei. 
Some of these cells show pale-blue or lilac cytoplasm, while others 
in addition contain dark-lilac or deep-purple granules. 

Mast cells resemble the ordinary polynuclear leukocyte, and 
in addition display coarse spheric granules, which are stained 
dark-blue, purple, or at times blackish. 

Myelocytes contain purplish or dark-blue nuclei. In the 
cytoplasm are seen numerous dark-lilac or reddish-lilac granules. 

Blood-plates appear as small round or oval bodies and are 
stained blue or purplish. These bodies show irregular margins 
and their substance contains fine blue or purplish dots. 

Preparation of Wright's Stain. — i. Prepare in an Erlen- 
meyer flask a one-half of one per cent, solution of sodium bicar- 
bonate, and to it add one per cent, of methylene-blue (Grubler 
"BX," "Koch's," or "Ehrlich's Rectified"). 

2. Place the mixture in an Arnold steam sterilizer for one hour. 

3. Remove and allow to cool; then pour into a large flask and 
add gradually (agitating after each addition) sufficient quantity 
of a i-iooo solution of yellow eosin (Grubler's soluble in water) 
until the mixture develops a purple color and a yellowish, metallic 
scum forms on the surface. A finely granular, blackish precipitate 
is now partially suspended in the mixture. Approximately one 
part of blue solution to five parts of eosin solution gives this 
result. 

4. Collect the precipitate on a filter-paper, dry thereon, and 
powder (see Jenner^s Stain). 

5. Place three-tenths of a gram of this dried stain in 100 c.c. 
of methyl-alcohol. 

6. Filter this saturated alcohoHc solution of the precipitate, 
and to the filtrate add 25 per cent, (one- fourth its quantity) of 
methyl-alcohol. 

Caution. — Wright's stain is permanent, and may be kept 
ready for use. It must be well corked, since evaporation of the 
alcohoL enhances precipitation, in which instance dark particles 
of the stain are found on the stained blood-film. 

Ehrlich's Tricolor Mixture. — Saturated aqueous solution of 
orange G, 6 c.c; saturated aqueous solution of acid fuchsin, 
4 c.c; to this is added, a few drops at a time, shaking between 
each addition, saturated aqueous solution of methyl-green, 6.6 
c.c; then add glycerin, 5 c.c; absolute alcohol, 10 c.c; and 
water, 15 c.c. Shake well for two or three minutes, and allow 



8o 



THE BLOOD. 




Fig- 39.— Wash- 
bottle. 



to stand twenty-four hours. Do not filter. Grubler's stains are 
necessary. 

This mixture is used daily in my laboratory, and meets dinical 
demands in every respect. It is well to remember, 
however, that it deteriorates rapidly, and is there- 
fore not satisfactory in the hands of the inexper- 
ienced, and also that it is often troublesome when 
used by its most ardent advocates. Certain 
admirable features are most prominent, such as, 
first, a single staining accompHshes the result; 
second, it is impossible to overstain the speci- 
men, as overstaining always depends upon faulty 
technic in the fixing of the specimen (underheat- 
ing). When films are brought to a temperature 
of 100° or 120° C, the heating should be con- 
tinued for a long time. When underheated, the 
specimen is brown or red instead of orange yellow; 
when overheated, a pale lemon yellow to the naked eye, and under 
the microscope, blurred. 

Method. — Place the shde or cover-glass in a forceps (Figs. 184- 
186), and Hft a few drops of the stain by means of a pipet, allowing 
the pipet to pass only a short distance below the surface of the Hquid. 
Caution. — Never shake the bottle containing the stain nor 
agitate the solution with the pipet. Cover 
the entire specimen with the stain, and allow 
it to remain for five minutes. Remove by 
washing in water from a wash-bottle (Fig. 39). 
At this point the specimen is to be dried 
between blotting-paper and mounted in Can- 
ada balsam. It is customary for the author to 
follow Ehrlich's stain with a 2 per cent, aqueous 
solution of methylene-blue apphed for ten seconds, and removed by 
washing. The specimen is then dried by heat or between blotting- 
paper and mounted in balsam. The methylene-blue brings out 
more clearly the nuclei of the cells. 

Method of Mounting. — The mounting of the specimen which 
has been prepared upon the shde is accomphshed as follows : 

1. Drying the specimen thoroughly in the air, by heat, or between 

filter-paper. 

2. Add a drop of balsam to the center of the specimen, care being 

taken not to cause bubbles. 

3. Allow the center of a clean cover-glass to fall directly upon 

the summit of the drop of balsam, which is spread by the 
weight of the glass. 



Fig. 40. — Slide label. 




THE ERYTHROCYTES. 8 1 

The slide may be examined immediately under a low-power 
objective and, if need be, immersion oil may be added to the center 
of the cover and a one- 
twelfth oil-immersion ob- 
jective brought into focus 
without destruction to the 
specimen. Slides should he 
immediately labeled (Fig. 40) 
and mounts permitted to 
rest upon their surface for 

twenty- four hours while the Fig. 41.— case for mounted slides. 

balsam becomes firm; after 

which they may be rung (see Method for Ringing, page 28). 
SHdes containing permanently mounted specimens should be 
placed in a case (Fig. 41) to rest upon their surface for twenty- 
four hours. 

THE ERYTHROCYTES. 

• 

The characteristic features of the erythrocytes in the blood 
of man are best described by the accompanying plates (2, 6, and 7), 
and their fidehty as to size, form, and the smoothness of their sur- 
faces is ever to be borne in mind ; since deviations from this stand- 
ard, when not the result of faulty technic, have a definite signifi- 
cance. They vary in nunlber from 4, 500,000 to 5 ,000,000 per cubic 
milHmeter, and 6,000,000 is not an uncommon finding in healthy 
young men. Menstruation, childbirth, and lactation diminish 
the number of red cells temporarily, and such diminution depends 
upon the capabiHty of the individual organism for cell regenera- 
tion. The number of cells is low at puberty. Either chronic 
or temporary dilution of the blood, as may result from the tak- 
ing of large quantities of liquid, lowers the number of cells, the 
specific gravity, and the hemoglobin. Hot and cold baths, ex- 
ercise, etc., from their effect upon the vasomotor system, may 
temporarily concentrate or dilute the blood of the peripheral 
circulation and cause it to show either an increased or diminished 
number of cellular elements, and the hemoglobin and specific 
gravity, will here be found in direct proportion to the degree of 
concentration or dilution. 

The blood is temporarily diluted after a meal at which Hquids 
have been taken Hberally. Fasting produces concentration of 
the blood and a temporary increase in the number of the red cells. 
Muscular persons, as a rule, have more red cells than fat indivi- 
duals. Again, malnutrition diminishes the number of red cells, 
and exhaustion may also be found to lessen the number of cells 



82 THE BLOOD. 

in certain cases. Age plays a prominent part as regards the 
number of red cells — the infant usually shows from 6,000,000 
to 8,500,000 erythrocytes per cubic milhmeter during the first 
week of life, while at the other extreme of life the cells may often 
be found below the normal, yet this is not constant. The in- 
fluence of season, race, and climate is unimportant in this con- 
sideration. 

ANEMIA. 

Anemia is a condition wherein there is a deficiency in the red 
cells or in the hemoglobin or in both, with or without change in 
the number of leukocytes, the total volume of blood, or further 
appreciable alteration in the chemic composition of either the 
cellular elements or the serum. For chnical study anemia may 
be divided into two classes, primary anemia and secondary anemia. 
In the first class are to be placed conditions where there exists 
an impoverishment, either of the whole blood or of any of its 
properties — the cause of such impoverishment being unknown; 
e. g., pernicious anemia, leukemia, and chlorosis. Secondary 
anemia includes conditions wherein the blood becomes impover- 
ished as the result of some known cause; e. g., diabetes, organic 
heart disease, tuberculosis, etc. 

Generally speaking, every anemia is secondary, since even in 
the first variety of our classification there must exist some cause. 
Sufficient tangible evidence is available, however, to warrant 
our regarding some forms of anemia as dependent upon a primary 
disease of the blood-making organs, or upon a specific process 
resulting in a destruction of one or more elements of the blood. 
It must be remembered that secondary anemia may sim- 
ulate closely, and is often not to be distinguished from, primary 
anemia; e. g., syphihs, gastric carcinoma, intestinal parasites 
(ankylostomiasis). Anemia identical with pernicious anemia 
may follow the more severe secondary forms; and, again, primary 
anemia may result from mental strain, pregnancy, fright, anxiety, 
and grief, in which cases it is termed "primary" (see Individual 
Forms), though in reality such anemia is "secondary." 

Chemistry of the Erythrocytes. — The analyses of Hoppe- 
Seyler, Schmidt, and Judell, though subject to criticism since 
the red cells were separated from the serum by the use of sodium 
sulphate and sodium chlorid, furnish the best available data for 
their approximate chemic composition. The specific gra\aty 
of the er\1:hrocytes is near 1.088, and they contain nearly 90 per 
cent, of oxyhemoglobin, a slight amount of globulin-like albumin 
which coagulates at 75° C, and a trace of cholesterin and lecithin. 



PLATE 2. 



Mm% . 



,-H , jH #A .:«j(i^ v^ 

^^■^ 1 2 

3 4 










ur.f\.Tft.A.iu^ 



5 6 

Blood-corpuscles of Various Animals. 



1. Frog's blood: Red cells nucleated, elliptic; white cells small, with indistinct 
rough margins. 

2. Pigeon's blood: Note the fine granules of the eosinophiles. 

3. Blood from umbilical cord of the fetus, showing nucleated red cells. 

4. Horse's blood: Note contour of red cells and also large granules of the 
eosinophihc leukocytes, one of which is mononuclear. 

5. Camel's blood: Note contour of red cells and irregularity in staining. No 
nucleated red cells were found. Two animals were studied. 

6. Normal human blood. (All specimens stained with eosin, hematoxylin, and 
methylene-blue. Obj. B and L. one-twelfth oil-immersion.) 



ANHYDREMIA. 83 

Such salts as phosphate of sodium, potassium, calcium, magne- 
sium, and chlorid of potassium are present. The predominant 
salt found in the blood-serum is NaCl. 

Increased Specific Gravity. — The specific gravity of the red 
cells according to Schmidt is increased in cholera, dysentery, 
and dropsy; and a chemic analysis shows that they partake 
of the changes which affect the serum — losing water, salt, and, 
lastly, albumin. 

Recently an attempt at estimating the normal contents of 
nitrogen for the red cells was made by v. Jaksch, who found wide 
variations in both health and disease. The dried residue of the 
red cells after the addition of sodium oxalate has been found by 
Biernacki* to be equal to from 29.28 to 30 per cent. This per- 
centage has been known to fall in cases of both essential and 
secondary anemia. 

Increas-ed Water. — The increased amount of water in the red 
cells has been observed in hydremia by the same author, who 
has contributed valuable data upon the relation of PjO^, Fe, K, 
and also sodium chlorid in the erythrocyte (see Hemoglobin). 

HYDREMIA. 

The hquid properties of the blood may be found increased 
in a variety of conditions. A temporary dilution of the blood 
is seen after the ingestion of large quantities of liquids, hypoder- 
moclysis, enteroclysis, and when large quantities of water have 
been extracted from the tissue (see Diabetes, page 68) ; but when 
found in connection with such conditions, hydremia is of limited 
significance. When the total volume of blood remains nearly con- 
stant and there is a loss of sohds or of the cellular elements, there 
must of necessity be an increase in the Hquid properties; therefore 
the blood of anemic persons is hydremic. 

Clinical Significance. — The blood of women is usually less 
rich in corpuscles and it is more hydremic than the blood of men. 
The blood of persons suffering from secondary anemia and of 
chlorosis shows about the normal amount of water in their serums. 
In pathologic conditions accompanied by dropsy the blood may 
contain more than the normal amount of water, which affects 
both the corpuscles and the plasma. 

ANHYDREMIA. 

A reduction of the total volume of blood with concentration 
of the soHds may result from both physiologic and pathologic 

* "Zeit. klin. Med.," vol. xxiv, p. 460. 



84 THE BLOOD. 

conditions; e. g.y violent exercise with profuse perspiration, and 
dry diet ; or after depletion, as is seen in dysentery, cholera asiatica, 
during certain stages of diabetes mellitus, and also in plethora. 
Anhydremic blood may contain an excess of fats. 



POLYCYTHEMIA. 

Polycythemia, a condition wherein the whole blood displays 
too many red corpuscles per cubic milHmeter, is physiologic in 
the new-born; and when pathologic, may be either general or local 
When general, blood obtained from any portion of the body 
discloses this phenomenon, which may exist as a result of dis- 
ease of the heart, obstruction to the circulation through the 
lung, congenital deformities of the heart, pressure from tumors, 
serous effusions, etc. The vessels of a given part of the body 
may be overcrowded with corpuscles as the result of mechan- 
ical appliances, — e. g., application of Esmarch's bandage, — 
from disease, or from vasomotor disturbance (local polycythe- 
mia). 

Cyanosis. — Cyanosis, resulting from whatever cause, may 
produce an increase in the number of cells in a given quantity 
(drop) of blood. A single drop of blood is an expression of the 
whole capillary circulation; yet capillary blood is richer in cor- 
puscles than is arterial or venous blood. Standards of the normal 
number of corpuscles per cubic miUimeter are estimated from 
capillary blood. I have seen the number of cells per cubic milli- 
meter reach twice that of the normal under such conditions. 
Blood collected from the capillary circulation of a paralyzed 
limb is unusually rich in cellular elements (local polycythemia). 

In chronic cyanosis the number of red cells will often be found 
to be from 7,000,000 to 10,000,000 per cubic milKmeter, and the 
hemoglobin is also far above the normal, varying from 120 to 
150 per cent. The specific gravity of the blood is Hkewise in- 
creased to from 1.065 to 1.080. The leukocytes are found to be 
less influenced by general chronic cyanosis, and usually vary from 
5000 to 16,000 per cubic miUimeter, rarely reaching 20,000. Osier* 
has reported a series of these cases wherein the maximum findings 
were red cells 12,000,000, leukocytes 20,000 per cubic millimeter, 
hemoglobin 165 per cent., and the specific gravity 1.083. 

Caution. — Cyanosis figures prominently in all blood counts 
made upon those suffering from severe anemia, or from such condi- 
tions as pneumonia, and where large serous effusions exist. I have 

* "Amer. Jour. Med. Sci.," Aug., 1903. 



POLYCYTHEMIA. 85 

repeatedly seen gross error resulting from failure to observe 
this important factor — cyanosis. In a case of pernicious anemia 
observed at the Philadelphia Hospital, blood from the lobe of 
the ear showed 1,840,000 red cells per cubic millimeter, while 
blood from the finger (hand cyanosed) showed 4,600,000. In 
lobar pneumonia with extensive consohdation, and in all con- 
ditions accompanied by cyanosis, we find the number of corpuscles 
per cubic milhmeter above the normal, when the total blood is 
really poor in cellular elements. 

After recovery from some prolonged illness, associated with 
severe anemia, regeneration of the red cells may be rapid and 
their number reach 6,000,000 per cubic milhmeter. In obesity 
I have seen the red cells reach 6,000,000 to 7,000,000 per cubic 
milhmeter, and, through the courtesy of Dr. J. M. Anders, a 
similar count was obtained from a boy eighteen years of age, who, 
formerly a resident of Philadelphia, had just returned from a 
year's visit to the tropics. The hemoglobin was 114; and the 
blood became normal after a six months' stay in Philadelphia. 

Burns. — Locke, in severe burns with recovery, found an 
increase in the erythrocytes of from 1,000,000 to 2,000,000 per 
cubic milhmeter to take place within a few hours. An increase 
of from 2,000,000 to 4,000,000 per cubic millimeter developed 
in fatal cases. 

Anesthesia. — Study of a series of cases reported in collabo- 
ration with Dr. J. M. Anders shows that polycythemia results 
from the administration of ether both in healthy men and in 
rabbits. These experiments consisted in counting the blood 
immediately before the administration of the anesthetic, and in 
making subsequent counts every twenty minutes during the 
administration of the ether; one hour after the ether had been 
discontinued, and several times daily until the blood returned 
to the normal. Here blood concentration was not accompanied 
by a decided rise in the hemoglobin (see Hemoglobin, page 41). 
In the study of human blood after the administration of ether 
it should be stated that the patients were not purged before ad- 
ministering the anesthetic; therefore the polycythemia observed 
depended upon the effects of the anesthetic, as did also the great 
reduction in the hemoglobin. Polycythemia resulting from the 
administration of ether was found to be of short duration, and 
was always followed by a decided reduction in the number of 
red cells, which reduction followed the fall in the hemoglobin (see 
Hemoglohin). 

Causes. — Temporary or permanent lack of fluid within the 



86 THE BLOOD. 

vessels causes concentration of the blood, and may result from 
the hmited use of hquids, purgation, diarrhea, dysentery, profuse 
sweating, vomiting, and the rapid accumulation of serous effu- 
sions. In a case observed in the Philadelphia Hospital with an 
extensive pleural effusion of some weeks' duration the red cells 
numbered 3,860,000. Forty ounces of fluid were removed from 
the pleura by aspiration, but at the end of twenty- four hours the 
effusion had reappeared in the pleura and at this time the red 
cells numbered 5,200,000 per cubic millimeter, an increase of 
1,340,000 cells. 

Great variation may be found in cases of phthisis when the 
blood is counted before and after a night-sweat. Thermic changes 
and drugs (suprarenal extract) may cause temporary concentra- 
tion of the blood, as does also a rise of the blood pressure. Con- 
centration depends upon interchange of contents between the 
blood-vessels and the tissues, but this change affects mostly the 
watery element of the blood ; the red cells taking but little, if any, 
part in the process. Cold induces an increase in the number of 
leukocytes in the peripheral circulation; yet evidence to show 
that there is an increase in the total number of leukocytes is 
wanting. Concentration dependent upon such causes exists 
but for a short time, since the general body tissues appear to give 
up sufficient hquid to restore this loss. 

Effect of Altitude upon the Blood. — The blood of persons 
Hving at high altitudes shows an increase of red cells per cubic 
miUimeter. This change is also manifest in those hving in low 
altitudes who make short sojourns among the mountains. The 
higher the altitude, the greater the increase in the number of cells. 
The hemoglobin, too, increases under such conditions, but this 
increase is not in proportion to that of the red cells. The blood 
of persons changing from near the sea-level to an altitude of several 
thousand feet displays great irregularity in the size and shape 
of the erythrocytes (microcytes) during the first few weeks' stay 
in such districts, but later these conditions disappear, and the 
hemoglobin reaches a level corresponding to the number of red 
cells. After returning from the mountains to the lowlands the 
blood count rapidly returns to the normal. Herrera and Lope 
collected data from the hterature, and in the following table 
I have abstracted liberally from their compilation, endeavoring 
to tabulate the average number of erythrocytes found to be repre- 
sentative of the normal at various altitudes : 



POLYCYTHEMIA. 



87 



1 Altitude. 


By Whom Observed. 


Red Cells 
PER Centi- 
meter. 


i 1 

1 Meters. Feet. 


Christiania Sea-level 

Paris 78 

Gottingen 148 

Tubingen 314 

Zurich 412 

Auerbach 400-450 

Reiboldsgrlin ' 700 

Arosa 1800 

City of Mexico 2256 

Colorado Springs.. 1824 
Morococha 4392 




255 

485 

1,030 

1.35 1 

1312-1476 

2,296 

5.905 

7.550 

6,000 

14,409 


laoche 

Hayem 

Schapper 

Reinert 

Stierlin 

Wolf and Koppe 

Egger 

Herrera and Lope 

Campbell and Hoagland 

Viault 


4,970,000 
5,000,000 
5,225,000 
5,322,000 
5,752,000 
5,748,000 
5,970,000 
7,000,000 
6,500,000 
5,700,000 
8,000,000 



A slight increase may result from latitudinal variations. 
Clinically, we not only observe an increase in the number of red 
cells and in the density of the blood of persons residing at elevated 
regions, but hand-in-hand with these phenomena there develop 
increased density of the urine, milk, body liquids, and diminu- 
tion of the intravascular tension of the blood. A number of theories 
have been advanced concerning the production of the polycy- 
themia of altitudes, but it appears plausible that polycythemia 
and its concomitant phenomena result from diminished barometric 
pressure, which lessens the amount of oxygen or oxygen pressure. 
The red cells being the hemoglobin carriers of the body are the 
first of the body tissues to manifest this change, and their increase 
in number bears sufficient close relation to the degree of altitude 
to suggest that the increase is just sufficient to meet the demands 
made by the general body tissues for oxygen. The time needed 
to establish this equilibrium is quite short. Campbell and Hoag- 
land* obtained the following counts fronl healthy individuals living 
at an altitude of 6000 feet, who were then transported to eleva- 
tions of 10,000 and 14,147 feet, and returned to the starting-point: 







6000 Feet 






10,000 Feet. 


14,147 Feet. . 


6000 Feet. 


Sex 


Age 


W^eight 


Pulse 


Count 


Pulse 


Count 


Pulse 


Count 


Pulse 


Count 


Male 


44 


1 189 


78 


5,760,000 


84 


6,070,000 


84 


6,100,000 


78 


5,790.000 


" 


27 


150 


80 


6,420,000 


104 


6,440,000 


96 


6,510,000 


82 


5,840,000 


" 


17 


135 


,80 


5,740,000 


80 


5,700,000 


84 


5,730,000 


78 


5,670,000 


" 


lb 




82 


6,150,000 


88 


6,280,000 


80 


6,390,000 


80 


5,970,000 


" 


19 


160 


90 


6,040,000 


84 


6,150,000 


88 


6,240,000 


8,5 


6,420,000 


" 


18 


145 


60 


5,890,000 


62 


6,750,000 


78 


6,960,000 


60 


5,500,000 


■ 


19 


120 


80 


5,680,000 


86 


6,340,000 


92 


6,380,000 


78- 


5.575,000 


Female 


40 


123 


78 


6,120,000 


80 


6,105,000 


88 


6,485,000 


76 


5,700,000 




51 


112 


84 


5,480,000 


88 


6,670,000 


90 


6,170,000 


80 


5,090,000 




20 


140 


84 


5,170,000 


88 


5,790,000 


9» 


5,955,000 


82 


5,790,000 


Average 


27 


1 142 


80 


5,845,000 


84 


6,229,500 


88 


6,292,000 


78 


5,734.500 



* "Amer. Jour. Med. Sci.," vol. cxxii, p 654. 



88 THE BLOOD. 

A rise of 50,000 red cells per cubic millimeter followed each 
additional 1000 feet of altitude. 

Polycythemia of Poisons. — Carbonic Oxid and Phosphorus- 
Poisoning. — After poisoning with CO the number of both red 
and white cells is increased, but here there is not a drawing away 
of the hquid properties of the blood. In acute phosphorus-poison- 
ing the number of red cells is often greatly increased, which in- 
crease may be explained, in part at least, by the occurrence of 
profuse vomiting. For description of Polyglobuha see p. 524. 

SECONDARY ANEMIA. 

Early in the course of secondary anemia there is but slight, 
if any, diminution in the number of erythrocytes, but as a rule 
each cell is pale (poor in hemoglobin), and yet all the cells may 
not share this loss. There is often found an unequal distribu- 
tion of hemoglobin, certain cells appearing pale, while others are 
normal, of small size, and Hght in weight, as shown by a low specific 
gravity. Such anemia commonly results from unhygienic sur- 
roundings. As the condition progresses there is to be observed 
merely an exaggeration of the changes above mentioned, and 
in addition many of the cells become deformed and irregular 
in size, var}'ing from that of mere dwarfed cells to giant cells, 
many of which display great irregularity of outHne (poikilocytes). 
The following text in conjunction with plate 3 will explain the 
characteristic features of the various abnormal erythrocytes. The 
several degenerative changes to which the red cell is subject may 
be classified as follows: 

I. Alterations in viscosity. 
11. Endoglobular changes or simple decoloration. 

III. Changes in the shape, size, and motility. 

IV. Atypical staining properties. 
V. Granular basophilia. 

VI. Total necrosis and disintegration. 

VII. Megaloblastic forms. 

Many of these changes in the erythrocytes may be seen to 
take place outside the body; and under pathologic conditions 
there are to be found cells displaying such abnormahties. 

Viscosity. — This property of the blood is detected by col- 
lecting fresh blood upon a shde and permitting it to be exposed 
to the air for a short time, when with advancing coagulation the 
greasy, slipper}' feel of fresh blood is replaced by a vary^ing degree 
of tenacity or stickiness (viscosity). 

Rouleaux Formation. — Should the viscosity be increased 
{hyperviscosity), the er}^throcytes instead of forming rouleaux — 
when the red corpuscles agglutinate one upon another hke a 



PLATE 3. 








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Various Forms of Erythrocytes. 

I, Normal erythrocytes; 2, karyokinetic changes in the nuclei of erythrocytes; 
3, pigmentation of the nuclei of erythrocytes; 4, polychromatophilia in nucleated 
erythrocytes; 5, megaloblasts; 6, microblast; 7, polychromatophiUa of macrocytes; 
8, microcytes; 9, macrocytes; 10, poikilocytes. At the lower margin of the picture 
is seen a basophilic leukocyte. (From blood of a child studied at Pennsylvania 
Hospital. Obj. B. and L. one-twelfth oil-immersion). 



11 



SECONDARY ANEMIA. 89 

column of coins — appear in dense irregular aggregations, and 
when a cell is found separated from these masses, it may be greatly 
distorted. When the viscosity is greatly diminished (hypovis- 
cosity), the erythrocytes are found singly, floating free in the plasma, 
and showing little or no tendency to rouleaux formation. The 
viscosity of the blood is influenced largely by the erythrocytes, 
yet the viscosity of the serum is a factor of importance. 

Estimation. — The viscosity of human blood is estimated at 
about five times that of distilled water. The viscosity of a blood 
ha\ing a specific gravity of from 1.045 to 1.055 is expressed by 
the figure 5.1, which is in comparison with that of water (i). 
To determine this point both fluids must be at a temperature of 
38° C. A close relationship between the degree of viscosity and 
the specific gravity does not exist, yet collectively speaking the 
lower the specific gravity of the blood, the less marked its adhesive- 
ness. 

Clinical Significance. — The viscosity of the blood is increased 
by a diet largely nitrogenous, exposure to the action of snake 
venom, * and by contaminating the fresh blood with serum from 
patients suffering from chlorosis, leukemia, or pernicious anemia 
(Stengel). In the severe anemias the non-adhesiveness of the 
erythrocytes is apparent. 

Endoglobular Changes (Simple Decoloration). — Decolora- 
tion of the erythrocytes is a most common feature of the blood 
in mild anemia when there is but slight involvement of either the 
hemoglobin or the cellular elements. Decoloration begins as 
a symmetric enlargement of the normally fighter area at the 
center of the cell and progresses toward the periphery. Such 
cells soon lose their normal biconcavity, and where decoloration 
progresses the cell is converted into a mere shell whose margin 
shows a faint color due to the persistence of hemoglobin {achro- 
macyte or shadow cell) . Areas of pallor may be distributed through- 
out the cell when there is a dissemination of the degenerative 
process; such areas are of various forms and sizes, outlining the 
stroma of the cell from which the hemoglobin has been removed. 
Areas of pallor in the erythrocyte have a selective affinity for basic 
dyes: e. g., thionin, by which they are briUiantly stained (see 
Basophilia, page 91). Normally, these changes occur in from thirty 
minutes to an hour after the blood has been withdrawn from the 
vessels, but in pathologic conditions they may be seen immediately 
after the blood is withdrawn, and it is supposed that they exist 
within the vessels. 

Changes in Shape, Size, and Motility. — Poikilocytosis 

* Weir Mitchell, "N. Y. Med. Jour.," vol. vi, p. 289. 



90 THE BLOOD. 

and crenation consist of decided irregularity in the form of the 
erythrocytes. Crenation is produced by a portion of the cell 
becoming looped and one or more points projecting from it 
(serrated margin). These points may become prominent, and 
in time the entire cell assumes ameboid movements. Such move- 
ments when they occur in rapid succession are responsible for 
the various shapes of the corpuscles (poikilocyte, see Plate 3). 
The ameboid motion of the erythrocytes has been studied at length 
by Hayem, but does not bear sufficient chnical significance to 
warrant description in this chapter. It may cause portions of 
the cell protoplasm to break from the corpuscle (schistocyte), 
and these particles after floating in the plasma for a time become 
spheric and resemble miniature erythrocytes (dwarj-cells). 

Brownian movement, a pecuHar vibration of the protoplasm, 
which is a feature of healthy blood, should not be confused with 
the movements resulting from crenation. In malaria there is 
also a Brownian movement of the pigment. In pernicious anemia 
there is a tendency for the red cells to become oval or elliptic, 
and poikilocytosis is also pronounced, but oval cells may be found 
in small numbers in the normal blood, while in any form of anemia 
they are increased. 

Caution. — When deformity in the cells depends upon faulty 
technic, the spicules extend from the same side of the cells or 
they point in one direction. 

The megalocyte or macrocyte (Plate 3) is an extremely 
large cell, between 12 and 20 ijl in diameter, and is the immediate 
successor of the megaloblast after its nucleus has been absorbed. 
Its stroma is usually deficient in hemoglobin (Plate 3) and is 
likely to possess polychromatic properties. This giantism of the 
erythrocyte maybe the result of imbibition of fluid from the plasma, 
as is suggested by its dropsical appearance. Another theory pro- 
mulgated is that its antecedent was a megaloblast of exceptional 
size. 

Clinical Significance. — Macrocytes are found in the blood of 
secondary anemia, where megaloblasts are conspicuously absent. 
They are to be found in blood showing megaloblasts. (Plate 6.) 

The microcyte is a spheric erythrocyte from 3 to 5 ,« in diam- 
eter, having a deeply colored stroma. The smaller of these 
cells are known as "Eichhorst's corpuscles." They are of dis- 
putable chnical significance. 

Atypical Staining Properties. — The normal erythrocytes 
have decided affinity for acid stains, but changes capable of pro- 
ducing alterations in the form and size of the cells probably cause 
certain staining abnormalities. Portions of the protoplasm may 



PLATE 4. 



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V 



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N O 






'd o 

(U 

bc q 



7 ^-^ 

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SECONDARY ANEMIA. 9I 

at times take the basic dyes {punctate basic degeneration) — as is 
exemplified in the blood of lead workers (Plate 4). Again, the 
cells may be colored by two, three, or more stains that may be 
contained in the staining mixture. This condition is known as 
polychromatophilia ; its causal factors are undetermined, and 
chnically it points to a high grade of anemia. Certain sections 
of the cell may stain deeply, while the remaining protoplasm is 
but feebly stained, and at times the entire cell merely stains as 
a capsule or ring, while its center is clear; or, the cell may have 
Httle or no hemoglobin, and appear as a shadow with an indistinct 
margin {shadow cell). 

Cabot^s Ring-bodies. — Cabot * has described ring-shaped 
bodies in the red cells which, when stained by eosinate of methylene- 
blue dissolved in methyl-alcohol, appear bright red in contrast 
to the surrounding protoplasm, which is pale yellow. These 
bodies occur in lead-poisoning, pernicious anemia, and lymphatic 
leukemia. Their clinical significance remains questionable. 

Granular basophilia or "punctate basic degeneration" 
is a condition characterized by small areas of degeneration dis- 
seminated throughout the protoplasm of the erythrocyte. In 
the stained specimen they are colored by the basic dyes (thionin, 
methylene-blue, and hematoxyhn). After staining with a solu- 
tion of carbolated thionin for five minutes they become quite 
conspicuous when studied under a one-twelfth oil-immersion ob- 
jective. They commonly assume the character of small amor- 
phous or oval granules, though short rods and spicules are also 
to be seen (Plate 4). 

Clinical Significance. — Basic degeneration is to be observed 
in most high grades of anemia, but is found abundant in the blood 
of lead workers. t Judging from current literature, there is suffi- 
cient evidence to show that these granules are not the product 
of nuclear fragmentation or of debris. The observers referred 
to have demonstrated in granular erythroblasts signs of active 
karyomitosis. These granules are to be found normally in the 
blood of embryonic mice,t and cats; also in developed rabbits, § 
squirrels, and guinea-pigs. Personally, I have observed it in the 
blood of- lead workers, || pernicious anemia, pulmonary tuber- 
culosis, and malaria. Stengel observed these granules in the 
blood of eleven out of eighteen chlorotics examined. 

* "Jour. Med. Research," Jan., 1903. 

t Stengel, White, and Pepper, "Amer. Jour. Med. Sci.," Sept., 1900; also 
1902, p. 873. 

X Pappenheim, "Inaug. Dissert.," Berlin, 1895. 
^ Ehrlich, "Die Anamie," Wien, 1900. 
II "Phila. Med. Jour.," Sept. 27, 1902. 



92 THE BLOOD. 

Necrosis. — Erythrocytic necrosis and disintegration are caused 
by exposure of normal blood to the air for from three to four hours. 
In pathologic blood such changes may be due to an increased 
toxicity of the plasma or to a lowered cell resistance, — in which 
instances the red cells are highly susceptible to injury by the 
plasma, — or by extraneous diversion. These changes may be 
observed in pathologic blood immediately after it is withdrawn, 
and are significant of a more severe type of anemia than is simple 
decoloration (Plate 6). 

Any or all of the above varieties of erythrocytes may be tound 
in a single case of secondary anemia, and the frequency with 
which such cells are to be found is governed by the severity of the 
existing condition. The third stage of secondary anemia presents, 
in addition, a shght and, at times, rather marked decrease in 
the number of the red cells per cubic millimeter. In the fourth 
or last stage of this condition we have, in addition to the other 
phenomena manifest, the presence of nucleated red cells, of which 
there are three varieties, normoblasts, megaloblasts, and micro- 
blasts. Nucleated erythrocytes are normal in the blood of rep- 
tiles, birds, and in the umbilical cord of the human fetus (see 
Plate 2). 

Megaloblasts. — The megaloblast is an abnormally large 
nucleated erythrocyte which is not found in the blood of healthy 
adults nor in the bone-marrow, and is a direct antecedent of the 
megalocyte, into which it is transformed by the absorption of its 
nucleus. It is often present in the marrow of the fetus and in 
the marrow from severe forms of anemia. Ehrlich was the first 
to describe this cell as characteristic of the fetal type of anemia. 

Clinical Significance. — The presence of megaloblasts in the 
blood may be regarded of serious prognosis, and a sign of de- 
generation of the hematopoietic organs, including defective hemo- 
genesis of embryonal nature; though not of necessity does a fatal 
issue ensue. Megaloblasts appear in the blood of the severer 
forms of secondary anemia, especially that produced by the 
ankylostoma (Uncinaria duodenale) , the bothriocephalus, and nitro- 
benzol poisoning, when they constitute a large percentage of the 
nucleated red cells. They are fairly characteristic of pernicious 
anemia. I have also seen them present in the blood after severe 
puerperal hemorrhage; and nucleated red cells whose size is but 
shghtly above that of the normoblast are not an uncommon find- 
ing in anemia. 

Description. — The typical megaloblast varies from 11 to 
20 /J. in diameter. It frequently shows evidence of degeneration 
in its protoplasm, as sweUing, unevenness, flaws, and cracks 



SECONDARY ANEMIA. 93 

which do not stain deeply (see Plate 3). The nucleus is, as a 
rule, large, occupying the greater portion of the cell, and, in 
striking contrast to the nucleus of the normoblast, it generally 
stains pale but evenly throughout (see Plate 3). Exceptional 
cells are to be found, and in the blood of a patient seen at the 
Pennsylvania Hospital, through the courtesy of Dr. J. AlKson 
Scott, many uncommon forms of megaloblasts were represented 
(see Plate 3). Surrounding the nucleus there is often a clear 
narrow ring outside of which the protoplasm may stain rather 
deeply, while toward the margin of the cell the protoplasm, at 
times, presents a purpHsh tint {polychromatophilia) . 

In the blood just referred to it was very difficult to separate 
the various forms of nucleated erythrocytes and, in fact, there 
appeared to be no one cell predominant, while there was a great 
variety of atypical cells, as shown in plate 3. The experience 
of hematologists shows that under all conditions megaloblasts 
cannot be distinguished from normoblasts by any one or by any 
methods ; and that border-hne cells are at times equally numerous 
with those characteristic of either type. Pappenheim regards 
the structure of the nuclear net-work as the most valuable dif- 
ferential point, but this is often difficult to detect. The majority 
of megaloblasts are young cells displaying large pale nuclei, and 
the bulk of the normoblasts older cells, presenting smaller nuclei, 
which stain more deeply. These features appear to be sufficient for 
practical differentiation. From a clinical point of view a most 
striking feature is that of a child whose blood presented these 
changes and who made an uneventful recovery (see Plate 3) — 
infantile anemia. 

The normoblast is a nucleated red cell which corresponds in size 
to that of the normal red cell, is conceded to be its antecedent, and is 
to be found in the bone-marrow of healthy individuals and more 
plentifully after great depletion of the body fluids. It is regarded 
as the younger stage in the Hfe of the red corpuscle, and is rarely 
seen in the healthy peripheral blood. 

Clinical Significance. — The appearance of normoblasts in 
the peripheral blood is suggestive of a decided production of the 
normal erythrocytes by the marrow, and that in this attempt 
to supply the demand made upon the marrow, certain cells are 
forced into the circulation before they are fully matured and have 
extruded their nuclei. Plate 6 will illustrate the various forms 
of normoblasts. Free nuclei are occasional findings. The 
nucleus may be stained evenly throughout — pale, dark, or present 
small, highly refractile dots. Two nuclei are usually connected 
by a feeble cable. Rarely the nucleus is located upon the margin 



94 THE BLOOD. 

of the cell (Plate 5); again, partially extruded; and when com- 
pletely within the cell, may assume almost any shape. 

The microblast is a small erythrocyte whose nucleus is less 
liable to variation than is that of the normoblast (Plate 3). The 
nucleus stains deeply and occupies the greater portion of the cell, 
leaving a thin band of protoplasm surrounding it. 

Oligemia (Quantitative Anemia). — Oligemia signifies a 
reduction in the total quantity of the blood. It usually results 
from extensive hemorrhage, and is temporary, since water is 
extracted from the tissues to restore the total volume of blood to 
that of the normal. During the existence of oligemia the vessels 
contract, and thus accommodate themselves to the lessened quan- 
tity of blood. 

Melanemia. — Melanemia is a condition in which dark pig- 
ment-granules appear in the circulating blood, and is noted in the 
blood of malaria and rarely in that of other febrile conditions. 
The yellowish or blackish granules of pigment are seen in the 
plasma or in the bodies of the leukocytes. 

NORMAL LEUKOCYTES. 

The figure commonly accepted for the healthy adult is 7500 
cells per cubic miUimeter, but this will be found to vary greatly 
in such conditions as malnutrition, time of day, exercise, influence 
of digestion, hot or cold baths, etc. Other conditions influencing 
the number of leukocytes will be considered under the special 
headings of leukocytosis or leukopenia. 

The terminology here becomes very confusing, and has re- 
sulted partly from the theory of the origin of the cell ("lympho- 
cyte"), partly from the characteristics of the "nucleus" ("poly- 
morphonuclear"), and, again, from the affinity displayed for 
certain anihn dyes ("eosinophihc," "neutrophihc"). The per- 
centage of the various forms of leukocytes will be found to deviate 
moderately in the healthy adult from the following table: 

Two sources are now accepted: 

f I. Polymorphonuclear neutrophils. 

(A) The myelogenic group (from the J 2. Eosinophils, 
bone-marrow) | 3. Large mononuclears (Ehrlich). 

L 4- Mast cells. 

(B) The lymphogenous group (from ade- | Lymphocytes, large and small, 
noid tissues) J 

Small lymphocytes 20 to 30 per cent. 

Large lymphocytes 4 " 8 

Polymorphonuclear neutrophils 62 "70 " " 

Eosinophils 0.5 " 4 

Mast cells 0025 " 0.5 " '" 



NORMAL LEUKOCYTES. 95 

Infants show a high percentage of lymphocytes (50 per cent. 
or more), while the polymorphonuclear elements are correspond- 
ingly reduced in number to from 20 to 40 per cent. 

Composition of the Leukocytes. — All efforts to ascertain 
the chemic composition of the leukocytes have been made by 
using pathologic blood (leukemic), from lymphoid tissue, or from 
pus, and it must be admitted that the chemic analyses of leuko- 
cytes obtained from such sources are subject to variation. 
LiHenfeld,* in his analysis of lymphoid tissue, probably gives us 
the most rehable data. Pus, which but Httle concerns us in this 
chapter, has been found to contain a number of different forms 
of albumin, including Bence-Jones' albumose. In leukemic 
blood recovered from the cadaver are to be found fatty acids, 
lecithin in excess, and glycogen. Nucleins are a variety of bodies 
which may be obtained either from animal or vegetable cells 
after digestion with pepsin. These are fairly insoluble in alcohol, 
water, and ether; they give the biuret and Millon's reactions 
(see Urine ^ page 217). They hold an abundance of phosphorus and 
iron, and their tinctorial properties facihtate in distinguishing 
them from the basic albumins; when boiled with dilute acids, 
give nuclein bases; and when treated with alkahs, albumin and 
nucleic acid result. 

Lymphocytes. — These cells are generally divided into two 
classes, large and small (Plate 9). The first variety ranges in 
size from shghtly below to moderately above that of the normal 
red cell, and the greater portion of its body is occupied by a rather 
compact, often coarsely reticulated, spheric nucleus, surrounded 
by a narrow band of strongly basophilic protoplasm, which is 
at times homogeneous and again reticulated. Protoplasmic 
granules are not present. 

The large forms, which vary in size from above that of the 
normal erythrocyte to that of the polymorphonuclear leukocyte, 
will be found to possess in a general way features characteristic 
of the smaller form. At times, however, the reticulum of these 
cells shows nodular thickenings often resembhng protoplasmic 
granules. The nucleus may show faint rings, suggestive of 
nucleoh, and nodular thickenings. A spheric nucleus is common 
to normal blood, but in pathologic conditions strongly basophihc 
and also hyaline lymphocytes are to be found, certain of which 
present indented or subdivided nuclei (see Leukemia, 'pa.ge 129). 

Large Mononuclears. — This cell is but shghtly above the 
size of the large lymphocyte, yet occasionally it is noted to be the 
largest cell of normal blood. The protoplasm is mildly basophihc, 

* "Zeit. f. phys. Chem.," vol. xviii, p. 473; also vol. xx, p. 155. 



96' 



THE BLOOD. 



finely reticular, displaying nodular thickenings or questionable 
granules. Its nucleus is vesicular, showing granular thickening 
in spots and granules resembHng a central nucleolus. The 
nucleus may be circular, horseshoe-Hke {transitional leukocyte) ^ 
or, less often, elongated (Plate 8). 

Polynuclear Forms. — This variety of leukocyte is, as a rule, 
about two or three times the diameter of a normal red cell. Its 
protoplasm is distinctly reticulated, displaying at various points 
of the reticulum many neutrophilic granules. As a rule, the pro- 
toplasm is mildly basophihc, displaying nodular thickenings here 
and there when stained with methylene-blue (Plate 5). The 
nucleus is elongated, constricted, and often distorted so as to 
form three or more rather distinct lobules, which upon careful 
study are found to be connected by narrow bridges or threads 
of nuclear substance. These more or less isolated portions of 
the nucleus are often shghtly granulated, displaying one or more 
central nodular thickenings, and rarely, indeed, are the various 
portions of the nucleus entirely separated. To this variety of 
cell the terms polynuclear, polymorphonuclear, and polymorpho- 
nuclear neutrophils are applied. Occasionally, cells are to be seen 
which display a decided affinity for basophihc dyes, — ^^poly- 
nuclear hasophils^^ (see Plate 6), — and these are probably a 
direct descendant of the first embryonal leukocytes, as shown by 
a study of fetal blood. 

Mast Cell. — This is a coarsely granular basophilic cell which 
deserves special mention (Plate 7). It is supposed to have its 
origin in the lymphoid tissue. 

Eosinophil. — A form of leukocyte varying in size from a 
small lymphocyte to the polynuclear forms. Its distinctive fea- 
ture is that its protoplasm is more or less thickly studded with 
strongly acidophihc (red) granules. The nucleus is rather 
coarsely granular, displaying two or more lobes, and, as a rule, 
stains feebly with the basic dyes (Plates 7,8). It is not uncommon 
to find the cell-wall ruptured and numerous red granules scat- 
tered about the pale nucleus as though the result of an explosion 
(Plate 6). 

LEUKOCYTES IN DISEASE. 

An absolute and relative increase in the number of leukocytes 
(leukocytosis); an increase in a certain variety of the cells, with 
or without any marked change in other forms; an absence or a 
great diminution in the number of any variety of cell, with or 
without a relative increase in the total number of cells ; a decrease 
in the total number of cells (leukopenia), and the addition of a 



LEUKOCYTES IN DISEASE. 97 

new cell, the "myelocyte," of which there are two forms, — "myelo- 
cyte and eosinophilic myelocyte," — constitute the relative and 
morphologic deviations of the leukocyte induced by disease. 
Changes in both the relative proportion and in the number of 
leukocytes are caused by conditions on a par with those capable 
of exciting changes in the erythrocytes, and will be described in 
detail under the special headings of Leukocytosis and Leukopenia. 

Essential Feature. — A conception of the normal relation the 
different cells bear one to the other, and the recognition of the 
myelocyte, are all that are necessary to distinguish between the 
leukocytes of pathologic and those of physiologic blood. 

Myelocytes. — The myelocyte, though it differs widely from 
any other form of leukocyte found in normal blood obtained from 
the peripheral circulation, resembles in certain respects cells 
which physiologically are present. It is not characteristic of 
any one form of disease, and may be occasionally found in the 
blood from a variety of maladies which are on the border Hne, 
so to speak, between pathologic and physiologic states. The 
myelocyte (Plates 7 and 8) with Ehrhch's triple stain appears as a 
spheric cell w^hose protoplasm is nearly occupied by a pale-stained 
nucleus studded with neutrophihc granules. 

Great variation in the staining affinity of the different granules 
in the same ceil is often seen, and "there is prominent a basophilic 
portion w^hich becomes less and less marked as the cell grows 
older" (Cabot). Such basophihc properties are seen to be less 
marked in the polynuclear neutrophilic cells, yet even here con- 
siderable difference may be observed in the contiguous cells of 
the same field, and also of the adjacent granules of the same cell. 
The size and form of myelocytic granules are not unlike those 
found in polynuclear cells. Most important as a distinguishing 
feature of the myelocyte is its nucleus, which is single, and does 
not display the distortion characteristic of the polymorphonuclear 
neutrophils; but, on the contrary, is always spheric or egg-shaped, 
and in almost immediate contact with the cell-wall for a com- 
paratively large portion of its circumference. The spheric nucleus 
is commonly placed toward one side of the cell. It is necessary 
to distinguish the myelocyte from the large lymphocyte, which 
can be said to differ from it only in that it (the lymphocyte) is de- 
void of granules. 

Eosinophilic Myelocyte. — The eosinophihc myelocyte differs 
from the one described in containing eosinophihc instead of 
neutrophihc granules. Both this cell and the neutrophihc myelo- 
cyte are to be found in great numbers in the bone-marrow. They 
are hkely to display variations in the staining of their granules, 
7 



98 THE BLOOD. 

the nucleus to show the evidences of old age (vacuoles or mitosis, 
Fig. 47), since occasionally a cell is seen containing two nuclei. 
There is no other leukocyte capable of such great variation in size as 
is the myelocyte, which may vary in diameter from 10 to 20 //. 
This variation extends from far above the diameter of the poly- 
morphonuclear leukocyte to that of the lymphocyte. 

Clinical Significance. — Myelocytes are found in the blood of 
splenomedullary leukemia, lymphatic leukemia, after certain severe 
forms of intoxication, prolonged fasting, essential anemia, grave 
secondary anemia, and in a number of border-hne conditions. I 
have found them after prolonged ether anesthesia. 

Transitional Neutrophils. — These are neutrophihc cells 
which appear to occupy a position between a true marrow cell 
(myelocyte) and the polymorphonuclear leukocyte, and display 
a nucleus which shares certain characteristics common to each 
of these varieties. Their significance is undetermined. 

"Tiirck's Stimulating Form.'* — A variety of cell regarded 
differently by various writers. Weil describes it as resembling 
a myelocyte whose granules have been fused into a smooth, homo- 
geneous color which surrounds the nucleus. The protoplasm 
always stains deeply, appears homogeneous; yet there is con- 
siderable variation in the tint in different cells, ranging from purple 
to violet or brown. In the majority of our observations these 
cells are regarded as either myelocytes or as large lymphocytes, 
and are not uncommonly referred to as border-cells. Their 
presence usually accompanies diseases showing leukocytosis. 

Degenerated Leukocytes. — This form of cell is most com- 
monly met with in the blood of leukemia, yet it may be found 
elsewhere. The first impression received is that they are arte- 
facts — abnormalities in cell structure due to faulty preparation 
of specimen; but this can usually be disproved, since they do not 
occur in the blood of healthy individuals treated in the same 
manner. Degenerated leukocytes stain as a homogeneous mass, 
are structureless, appear to have lost their protoplasm, and their 
edges are ragged (karyolysis). Vacuohzation of both the proto- 
plasm and of the nucleus are not uncommon findings; while the 
large mononuclear cells display such degenerative changes as 
breaking up, pallor of the nucleus, structurelessness, and may 
appear as shadow cells. 

DIFFERENTIAL COUNTING OF THE LEUKOCYTES. 

The object here is to determine what percentage of the total 
number of leukocytes present belongs to each of the subvarieties 



DIFFERENTIAL COUNTING OF THE LEUKOCYTES. QQ 

of these cells previously described (page 94). In order that a fair 
estimation be gained, at least 600 leukocytes should be counted. 
This examination consists in classifying the leukocytes under their 
respective heads. It is this class of work alone which makes the 
mechanical stage most valuable; yet it cannot be said that this 
accessory to the microscope is necessary; though the use of such 
an instrument facilitates the making of a differential leukocytic 
count, and I beheve adds materially to the authenticity of the 
result (count). 

Method for Counting. — Bring a properly stained and mounted 
specimen into focus under an oil-immersion objective, and place 
at the right hand the following table, upon which to record each 
cell under its respective class. The slide is carefully moved until 
we have covered the surface of the smear, or at least sufficient 
of the surface to have counted in all 600 leukocytes. 

DIFFERENTIAL LEUKOCYTE COUNT. 

Name 

Residence 

Polymorphonuclear neutrophils 408 = 68.0 per cent. 

Large lymphocytes 30 = 5-° 

Small lymphocytes 108 = 18.0 

Large mononuclears 18 = 3.0 

Mast cells 3 = 0.5 

Eosinophils 15 = 2.5 

Myelocytes 12 = 2.0 

Eosinophihc myelocytes 6 = i.o 

Total 600 = loo.o '' " 

During the counting of 600 leukocytes there are found — 

{Normoblasts 4 
Microblasts 3 
Megaloblasts 3 

The estimation of the percentage of each variety of cells 
present in this given specimen of blood is accomphshed by using 
the number of each variety of cell found as the one factor, and 600, 
the number of cells counted, as the other. 

Nucleated Red Cells per Cubic Millimeter. — The number 
of nucleated red cells seen while counting 600 leukocytes is also 
recorded (see above); and the number per cubic millimeter is 
readily estimated in the following manner: 

Let a = number leukocytes counted, or 600 

" b = number nucleated red cells seen, or 10 

" c = number leukocytes per cubic milhmeter, ( r 12,000 

c or 12,000 X 2 — = 200, the number of nucleated red cells in one 

a or 600 

c.mm. of undiluted blood. 



lOO THE BLOOD. 

Counting. — In counting begin at the upper left-hand comer 
of the specimen, and cause the lens to traverse across the specimen . 
from top to bottom, moving the shde a sufficient distance to the 
right after each crossing of the slide so as not to include any of 
the cells which have been previously counted (Fig. 32). It requires 
but Httle practice until one becomes able successfully to manip- 
ulate the shde. The time necessary for making a differential count 
depends entirely upon the number of leukocytes found upon the 
smear, and when the leukocyte count is below 12,000, the procedure 
is tedious. 

BLOOD-PLATES. 

Blood-plates (Plate 13) appear as cohesive, circular or ovoid 
homogeneous bodies with irregular outlines, and are from one- 
third to one-half the diameter of the erythrocyte. They are 
devoid of hemoglobin and of nuclei, and are rarely seen in normal 
blood. Their number has been estimated by von Emden at 
from 180,000 to 250,000; Pruss gives the average as 500,000; 
and Kemp and Calhoun, 860,000 per cubic miUimeter. Blood- 
plates form a prominent constituent of white thrombi, and when- 
ever they are diminished, clot-formation is apt to be retarded, 
and the possibility of hemophiha or purpura may be suspected; 
also a lowered resistance of the erythrocytes. An increase in the 
number of blood-plates is suggestive of the development of thrombi. 

Clinical Significance. — In pernicious anemia they are dimin- 
ished and thrombosis is comparatively rare. An increase occurs in 
leukemia after hemorrhage, and in certain other grave afebrile ane- 
mias, and they are normal or increased in tuberculosis and pneu- 
monia. In such types of infection as erysipelas, malaria, and 
typhus, and in purpura and hemophiha, they are diminished, and 
in the latter condition at times absent. It should be borne in mind 
that only intravenous thrombosis is influenced by blood-plates, 
and that clot-formation outside the body is an entirely different 
phenomenon, depending upon the amount of fibrin present in the 
individual's blood. Opinions differ as to the origin of blood-plates. 

Chemic Composition of Blood-plates. — Lowit maintains 
that blood-plates are composed of globuhn; while Lihenfeld 
believes them to belong to the nucleo-albumins, and suggests 
that they result from the destruction of the nuclei of leukocytes. 



BLOOD DUST. 

Blood dust — "hemokonia" — is a constituent of both normal 
and pathologic blood, which has until recently received but 



LEUKOCYTOSIS. lOI 

little attention. It appears as small, round, colorless granules, 
which correspond in size and form to fine oil-droplets; their size 
ranges from one-fourth to one micromilhmeter in diameter. These 
granules are highly refractile bodies, displaying a rather rapid 
dancing motion, and are devoid of locomotion. Blood dust is 
insoluble in alcohol and in ether; does not stain by osmic acid, 
and has not been shown to contribute toward the formation of 
fibrin. The Hght of the Welsbach burner appears to assist in 
studying these bodies, which are also to be found in pus and in 
the fluid from the serous sacs. 



LEUKOCYTOSIS. 

Leukocytosis is a condition characterized by an increase in 
the number of leukocytes in the peripheral circulation over the 
number commonly found in the same individual, without a diminu- 
tion in the number of polymorphonuclear cells, but usually this 
variety shows both an absolute and relative increase over the 
number normally present. 

Physiologic leukocytosis appears some hours after the inges- 
tion of a meal rich in carbohydrates, and after exercise, mas- 
sage,- cold baths, parturition, during pregnancy, and in the 
new-bom. 

Pathologic leukocytosis follows hemorrhage, and in certain 
infectious diseases, as relapsing fever, Asiatic cholera, erysipelas, epi- 
demic cerebrospinal meninigitis, pneumonia, bubonic plague, yel- 
low fever (not constant), glanders, actinomycosis, acute articular 
rheumatism, scarlet fever, small-pox, diphtheria, folHcular tonsillitis, 
syphiHs (secondary stage), trichinosis (usually moderate), filariasis 
(early), mahgnant endocarditis, acute pancreatitis, gonorrhea, acute 
endometritis, cystitis (occasionally), acute pyemia, septicemia, 
cholangitis, cholecystitis, and shortly befoie death (terminal 
leukocytosis). It is seen in a variable degree in connection with 
inflammatory processes involving either the deeper tissues, vis- 
cera, or skin, as well as in certain forms of malignancy, lithemia, 
gout, toxemias and in lead workers where they fluctuate between 
9000 and 25,000 during the primary attack of colic* 

Among the more strictly locahzed processes that may cause 
leukocytosis are abscesses involving either the glands or other 
tissues, appendicitis, osteomyelitis, pyelonephritis and pyelo- 
nephrosis, perinephritic abscess, abscesses involving any of the 
viscera, locahzed peritonitis, epididymitis, conjunctivitis, proctitis, 
and any acute inflammation of the serous membranes. Leuko- 
cytosis is also a component feature of gangrenous stomatitis, noma, 
etc., and is often well marked in such cutaneous conditions as 

* Boston, " Phila. Med. Journal," Sept. 27, 1902. 



I02 THE BLOOD. 

pemphigus, herpes zoster, eczema, dermatitis, urticaria, pellagra, 
ichthyosis, and, rarely, in psoriasis. 

Toxic Leukocytosis. — For want of a better term the follow- 
ing conditions have been arranged under this head, which, though 
indefinite, explains in a measure, at least, the cause of leukocytosis 
in many of the conditions here grouped; yet these conditions are 
not always associated with leukocytosis — viz., acute yellow atrophy 
(hepatic), cirrhosis of the hver with jaundice, uremia, rickets, 
gout, ptomain poisoning, cinchonism, after intravenous injection 
of normal salt solution, illuminating-gas poisoning (Cabot), chloro- 
form anesthesia, ether anesthesia, and acute maniacal deHrium. 

Leukocytosis of Malignancy. — There appears to be some 
difference of opinion as to the true nature of the leukocytosis of 
malignant disease. Alexander* found the leukocytes to vary 
from 2360 to 21,700 per cubic millimeter in cases of malignancy 
of the breast, and not dissimilar results have been obtained by a 
number of observers in carcinoma of the stomach and of the 
rectum. Schneider found leukocytosis in 12 cases of malig- 
nancy. Osterspeyt detected leukocytosis in but 2 out of 12 cases 
examined. My own experience suggests that leukocytosis varies 
with the degree and stage of malignancy, also with its location, 
and with the presence or absence of ulceration and suppurative 
surfaces. The wide variation found in over 60 leukocyte counts 
made upon cases of mahgnancy renders it impracticable for me 
to draw any definite conclusions. 

Leukocytosis of Anesthesia. — T. L. Chadbourne,t in the 
study of 21 cases, found that there was always an increase of the 
leukocytes, resulting from the administration of ether anesthesia. 
Counts were made immediately before the anesthetic was begun 
and a second count taken after the ether had been continued for 
sixteen and two-third minutes. The average increase in the 
number of leukocytes was found to be 37.3 per cent, (the lowest 
6, the highest 73 per cent.). Differential counts were made upon 
5 of these cases and showed that the increase affected the poly- 
morphonuclear cells and the lymphocytes equally. A fact to be 
borne in mind is that each case presented some pathologic con- 
dition, and the majority of the cases showed over 10,000 leuko- 
cytes per cubic millimeter before anesthesia. Operation often 
appeared to cause a reduction in the number of leukocytes. 

A. von Lerber§ counted the leukocytes in loi cases, and found 
them to be increased after ether anesthesia in 96 instances. The 
remaining 5 cases should not be included, since a high-grade 

* "These de Paris," 1887. f "Inaug. Dissert.," Berlin, 1892. 

J "Phila. Med. Jour.," Feb., 1899, p. 390. | "Inaug. Dissert./' Berne, 1896. 



LEUKOCYTOSIS. IO3 

leukocytosis existed before anesthesia. In 35 instances the num- 
ber of leukocytes was double and in 23 triple the number found 
before ether. The effect of the operation is not considered in his 
estimation. Blake and Hubbard * studied 28 cases, making counts 
before and after ether anesthesia, and found the peripheral cir- 
culation to show no increase in the number of leukocytes. 

I secured permission from a healthy male, aged thirty-three 
years, to conduct the following experiments upon him. He had 
never taken ether as an anesthetic, always enjoyed health, and 
had abstained from alcohol. He was not prepared for the anes- 
thetic by purgation (studied with Dr. J. M. Anders) : 

Six hours after a meal and immediately before beginning the 
anesthetic, I found the hemoglobin to be 86 per cent.; red cells 
4,080,000; leukocytes 7600 per cubic millimeter. Upon staining, 
the blood was normal. After ether had been given twenty-five 
minutes (complete anesthesia, ten minutes) it was discontinued — 
hemoglobin 79 per cent., red cells 6,150,000, white cells 16,000. 
Microcytes numerous, all cells rather pale. One hour after 
ether had been withdrawn, hemoglobin 74 per cent., red cells 
4,170,000, white cells 9800. Many of the red cells stained as 
mere shadows, and their size varied. A differential count of 
600 leukocytes gave: 

Polymorphonuclear Si-97 per cent. 

Small lymphocytes 2.22 " " 

Large mononuclear i.ii " " 

Transitional 10.00 " " 

Eosinophils 0.38 " " 

Myelocytes 4-32 " " 

Twenty-four hours after ether (but little vomiting had occurred), 
hemoglobin 67 per cent, (loss of 19 per cent.), red cells 4,576,600, 
white cells 13,600. 

In collaboration with Dr. J. M. Anders I also conducted a 
series of experiments upon healthy persons and upon rabbits, 
and found a great reduction in the hemoglobin after ether 
anesthesia. Leukocytosis was also pronounced in many of these 
experiments, and the general course of the blood returning to the 
normal after anesthesia was found to be the same in man as in 
animals.^ It required from twenty-four to forty-eight hours for 
the restoration of the blood to normal.f 

Drugs. — :A variable degree of leukocytosis may follow the 
administration of drugs by mouth, subcutaneously, or by the 
rectum. By the first method, ether, chloroform, tincture of 
gentian, oil of peppermint, oil of anise-seed, camphor, thyroid 

* "Annals of Surgery," 1901. 

t Anders and Boston, "Proc. Phila. Col. Physicians," June, 1904. 



jQM THE BLOOD. 



extract, bicarbonate of soda, caffein, quinin, bismuth, and after 
purgation with castor oil, scammony, and podophylhn, the leu- 
kocytes are increased. Cabot* reports a series of instances where 
leukocytosis has followed toxic doses of opium, chloral, caustic 
potash, corrosive sublimate, belladonna, nitric acid, carbohc acid, 
arsenic, and alcohol. 

A similar phenomenon is observed after the intravenous 
administration of uric acid, pilocarpin, antipyrin, urate of soda, 
nuclein, nucleic acid, hemi-albumose, peptone, pepsin, tubercu- 
hn, pyocyanin, extract of bone-marrow, thymus gland, and spleen, 
all of which are followed by a sUght temporary reduction m the 
peripheral leukocytes, and later by leukocytosis. 

The degree of leukocytosis is often parallel to that of the local 
irritation produced, as is exempHfied by the leukocytosis follow- 
ing the subcutaneous injection of weak acids or alkahs; and from 
the local appUcation of mercury, antimony, croton oil, etc. Large 
doses of either bacteria or their toxins reduce the number of leu- 
kocytes; while moderate doses give no constant finding, since 
the individual animal resistance is capable of permitting or pre- 
venting wide fluctuations; but commonly a diminution m the 
leukocytes ensues, and is a precursor of leukocytosis. 

Leukopenia (hypoleukocytosis) is a condition when the 
number of leukocytes found in the peripheral circulation is below 
that of the normal for a given individual. Leukopenia may result 
from malnutrition, prolonged cold baths, hot baths; infectious 
conditions wherein there is no leukocytosis may present these 
phenomena; e. g., measles (early stage), rotheln, tubercular 
meningitis, la grippe, purely tuberculous conditions, typhoid 
fever (late in its course), and malaria. When the result of star- 
vation, and in typhoid fever, the number of lymphocytes is rel- 
atively increased. Leukemia when compUcated by an infection 
displays this phenomenon. Pernicious anemia, splenic anemia, 
Hodgkin's disease, the anemia of syphilis, ''Dum-dum" fever 
(tropical anemia with splenic enlargement), and hemorrhage may 

display leukopenia. ^ u i ^ 

Lymphocytosis.— Lymphocytosis consists of both an absolute 
and a relative increase in the number of circulating lymphocytes. 
This increase must be compared with the normal number of lym- 
phocytes for each individual m order to estabhsh the presence 
of lymphocytosis. Again, lymphocytosis may co-exist with an 
increase of the total number of leukocytes (lymphatic leukemia). 
The number of lymphocytes is high in the blood of healthy 
infants— 50 to 60 per cent.— during the first few weeks of extra- 
uterine hfe; and is also apt to be increased in many of the diseases 

*"Clin. Exam, of the Blood," fifth ed., pp. 415-419- 



LEUKOCYTOSIS. I05 

of childhood ; while in adults there are normally 20 to 30 per cent, 
of small and 4 to 8 per cent, of large lymphocytes. The increase 
may affect principally either the smaller or the larger lymphocytes, 
and it is not uncommon to find these cells quite uniform, rendering 
it impossible to classify them according to size (Plate 9). 

Caution. — Be slow to diagnose lymphatic leukemia in the 
young, since the blood of rickets, hereditary syphihs, scurvy, 
variola, diarrhea, gastro-intestinal disorders, malnutrition, and 
pertussis often shows an increase in the number of lymphocytes. 
During convalescence from exfoHating dermatitis, pertussis, and 
diarrhea, I have seen the number of lymphocytes equal 55 to 65 
per cent, of the total number of leukocytes. 

Clinical Significance. — In children the degree of lympho- 
cytosis serves as a fair index to the child's development in cases 
where it is possible to exclude other etiologic factors. It is also 
of limited value in diagnosing whooping-cough before the charac- 
teristic symptom appears. The large lymphocytes are increased 
in certain splenic tumors, and in measles after the temperature 
has reached the normal. 

False Lymphocytosis. — The blood of adults not infrequently 
shows false lymphocytosis, a condition wherein the apparent 
increase in the number of lymphocytes results from the absolute 
diminution of the polymorphonuclear cells; and is observed 
in general debihty, pernicious anemia, chlorosis. Graves' disease, 
syphihs, cervical adenitis, hemophiha, goiter, and typhoid fever. 

Absolute Lymphocytosis. — Absolute lymphocytosis is the 
term used to denote a condition wherein the total number of leuko- 
cytes is increased, and there is an abnormally high percentage 
of lymphocytes present. It is characteristic of lymphatic leu- 
kemia; and has been observed by Cabot in two cases of broncho- 
pneumonia comphcating whooping-cough. 

In a case of exfoHating dermatitis (boy of eight years) studied 
at the Philadelphia Hospital in 1897, I found the leukocytes to 
number 55,000 to 65,000 per cubic milhmeter, 60 per cent, of 
which were lymphocytes. Three months later the leukocytes 
were practically normal. 

Absolute lymphocytosis occurring in conjunction with glan- 
dular enlargement constitutes the diagnostic feature of lymphatic 
leukemia. Cabot regards lymphocytosis with eosinophilia as 
suggestive of obscure syphihtic disease. Lymphocytosis may be 
excited by thyroid extract, pilocarpin, and tubercuhn. 

Eosinophilia. — A condition of the blood characterized by 
an increase in the number of eosinophils (see Plates 5-7 and 8, 
eosinophils and eosinophilic myelocyte). 



Io6 THE BLOOD. 

Physiologic eosinophilia is observed during infancy and men- 
struation. 

Pathologic eosinophilia may be found in the following con- 
ditions: Fibroid bronchitis; bronchial asthma, and when dysp- 
nea is a prominent feature where they have been known to 
reach 50 per cent, of the total number of leukocytes (see Spu- 
tum, page 445); and in certain acute and chronic cutaneous 
maladies, as urticaria, where I have seen them equal 62 per cent.; 
prurigo and psoriasis, where they were noted to reach 17 per 
cent, by Cannon, and 22 per cent, in a case observed personally 
at the dermatologic chnic of the Medico- Chirurgical Hospital. 
I have also observed at the same clinic eosinophilia in connec- 
tion with herpes zoster, pemphigus, dermatitis, ichthyosis, and 
chronic eczema. In gonorrheal urethritis increasing eosinophilia 
suggests extension of the trouble to the posterior urethra. In 
prostatitis the eosinophils are often increased. 

Parasitic Eosinophilia. — Trichinosis, filariasis, and infec- 
tion with Bilharzia hasmatobia* may show a variable degree of 
eosinophilia early, but later eosinophilia becomes less marked, 
and may even be absent, as has been the course of a case of trich- 
inosis which I have been privileged to follow for a period of 
five years. Calvert I studied two cases of filariasis, in one of 
which the blood showed from 12.33 to 22 per cent, of eosino- 
phils; while the second presented from 6 to 20 per cent. Leuko- 
cytosis existed in both instances, varying from 26,666 to 14,000 
per cubic millimeter. 

Buckler concludes from a series of investigations that all 
varieties of helminthides are capable of causing an increase in 
the number of eosinophils in the blood. He found with infec- 
tion by the oxyuris 16 per cent, of eosinophils; ascarides, 19 
per cent.; ankylostoma, 72 per cent.; and Taenia mediocanellata, 
34 per cent. (Ehrhch and Lazarus, p. 429; see also Ankylostoma, 
page 143). 

Malignant Tumors. — Eosinophiha may be found in connec- 
tion with mahgnant growths, sarcoma commonly ranging from 
8 to 12 per cent.; but in lymphosarcoma the percentage may 
be greater. 

Eosinophiha may follow the removal of the spleen or when 
this organ fails to functionate. Hemorrhagic exudates and 
purpura haemorrhagica are often accompanied by a high-grade 
eosinophiha. In a case of chylous ascites (tubercular) I 
have found 38 per cent, of eosinophils in the peripheral circu- 
lation. Klein found 74 per cent, of eosinophils in the hemor- 

* "Lancet," Dec. 6, 1902, p. 1540. 

t "Johns Hopkins Hosp. Bui.," Jan., 1902, p. 23. 



BACTERIOLOGY OF THE BLOOD. I07 

rhagic pleural effusions, with an increase in the number found in 
the peripheral circulation. Eosinophilia is a common feature 
of myelogenic leukemia (see Leukemia, page 130). In leprosy 
I found 8.7 per cent, of eosinophils.* 

Medicinal eosinophilia may follow phosphorus-poisoning 
and, according to Taylor, the administration of nuclein and 
pilocarpin. The eosinophils are increased to 9 per cent, by the 
administration of camphor. During the height of the course 
of infectious fevers the eosinophils are found to be diminished, 
and at times absent — scarlet fever and rheumatic fever serving 
as exceptions to this rule. They are also diminished by the 
administration of ether as an anesthetic (Anders and Boston). 

During the post-febrile period it is common to find an increase 
in the number of eosinophils, which ranges from 9 to 90 per cent, 
of the total number of leukocytes. 

Clinical Significance. — Eosinophilia is of great service in 
diagnosing trichinosis, filariasis, tumors connected with the 
genital tract, and has been found by me in leprosy. In malig- 
nancy it is usually conceded to follow the existence of metas- 
tasis, and when co-existent with lymphocytosis, favors obscure 
syphihs. An increase in the eosinophils accompanies the uric- 
acid diathesis. EosinophiHa may be regarded of favorable 
prognostic value when it develops during the course of scarlet 
fever, pernicious anemia, chlorosis, and after hemorrhage. In 
obscure tumors of the viscera eosinophiha tends to exclude maHg- 
nancy. 

Diminution of the Eosinophils (Hypoeosinophilia). — 
The eosinophils are diminished or absent during the height of 
acute fevers, as typhoid, diphtheria, pneumonia, la grippe, and the 
majority of febrile conditions which display leukocytosis during 
some part of their course, during digestion, and after vigorous 
muscular exercise. This diminution in the number of eosinophils 
does not depend upon high fever, since an increase may be 
observed in scarlet fever, rheumatic fever, and malaria. Hem- 
orrhage and mahgnancy are often associated with hypoeosin- 
ophiha, and it is said to follow castration (Neusser). 



BACTERIOLOGY OF THE BLOOD. 

There are valid reasons for the belief that initially most blood 
infections are local; that after a lowering of the normally present 
protecting power, the barriers are broken and secondary infec- 
tion ensues (bacteremia). Such invasion results in streptococce- 

* "Trans. Phila. Co. Med. Soc," Jan., 1903. 



Io8 THE BLOOD. 

mia, staphylococcemia, bacillemia, or diplococcemia. Among the 
bacteria that are to be found free in the circulation are the fol- 
lowing: Streptococcus, bacillus of anthrax, Bacillus enteritidis, 
Bacillus pyocyaneus. Bacillus proteus vulgaris, bacillus of glanders, 
bacillus of Friedlander, bacillus of tuberculosis, typhoid bacillus, 
paracolon bacillus, colon bacillus, bacillus of Sternberg, Bacil- 
lus pestis, Bacillus leprae, vibrio of cholera, spirillum of 
relapsing fever; and the Micrococcus melitensis, gonococcus, 
pneumococcus, Diplococcus intracellularis, Micrococcus tetra- 
genus, diplococcus of scarlatina (Class); and micro-organisms 
have been found in the blood in such diseases as chorea, 
purpura haemorrhagica, rheumatism, scurvy, sepsis, mumps 
(diplobacilli), etc. One observer reports having found a diplo- 
coccus in the blood of typhus fever. I v^^as unable to confirm this 
report in the study of two cases at the Philadelphia Hospital. 



THE REACTION OF BACTERIA AND THEIR PRODUCTS OF THE 

BLOOD. 

Many of the changes that appear in the blood, commonly 
regarded as being the effect of fever, are in reahty caused by the 
action of bacteria or their products; and such bacteria may be 
the direct cause of the disease from which the individual is suffer- 
ing. The researches of Bouchard, Gley, and others have shown 
that in the bodies of certain organisms (Bacillus pyocyaneus) 
and in their filtered products were substances capable of produc- 
ing a vasoconstricting action. This serves to explain the poly- 
cythemia present in certain febrile conditions (see Polycythemia, 
page 84). The injection experimentally of peptone, animal ex- 
tracts, tubercuhn, and pyocyanin produces in a similar manner con- 
centration of the blood. Grawitz* has detected decided variation in 
the density of the blood after the injection of pure cultures of 
diphtheria, the various pus-producing organisms, and the vibrio 
of cholera. The isotonic tension of the blood was found to be 
increased by small doses of toxins, while large doses, and even 
the injection of typhoid bacilh, produced an opposite effect. f 
The various products resulting from the development of bacteria 
in the human organism — ptomains, toxalbumins, and bacterio- 
proteins — are generally conceded to be the active and destructive 
agents of the albumins of both the blood and body tissues in all 
infectious conditions. Changes in the body tissues are not of 
necessity associated with fever. The chemotactic action of both 

* "Zeit. f. klin. Med.," vol. xxii, p. 411. 

t Bianchi and Mariotti, "Wien. med. Presse," 1894, No. 36. 



METHOD OF COLLECTING BLOOD. ICQ 

bacteria and their products upon the leukocytes is displayed 
through theproduction of leukocytosis (see Leitkocytosis.'^d,^^ lOi). 



METHOD OF COLLECTING BLOOD, 

1. Sterilize the skin of the flexor surface of the arm above 
and below the elbow, when an assistant should grasp the arm 
so as to prevent the venous return of the blood and thereby dis- 
tend the superficial veins. My own practice is to make an in- 
cision through the skin and allow the assistant to draw its edges 
aside by the aid of two tenacula, when it is possible to enter the 
vein directly and thus avoid possible contamination by passing 
the needle through the skin. 

2. Into the most prominent vein plunge a hypodermic needle. 
When the needle enters the vein, the blood usually begins to flow 
into the bulb of the syringe, and this should be 
gradually enhanced by withdrawing the piston 
slowly until about one-half cubic centimeter of 
the blood has been removed. Withdraw the 
needle quickly and apply a surgical dressing to 
the site of the wound. 

3. Immediately expel the blood contained in 
the syringe into tubes containing agar-agar which 
is heated to a temperature of 42° C. (just suf- 
ficient to liquefy the medium and not to interfere 
with bacterial growth). After the addition of one 
or more drops of blood to the tube, shake well, 
and stand in a cool place until the medium is '^' flask. ^^ 
soHdified. It is well to incHne the tubes shghtly 

in order to obtain surface growths. Tubes or flasks (Fig. 42) 
containing bouillon may be inoculated with the blood in this 
manner, and it will be found a most convenient method of inocu- 
lating tubes for plating. 

Personal experience favors the plan of mixing the blood with 
a Hquid culture-medium and then inoculating other tubes with 
this mixture. The only objection which can be raised to the 
diluting, of the blood before it is used for inoculation of tubes 
is the liabihty of contamination, but this danger, with our present 
bacteriologic technic, is reduced to a minimum. 

Caution. — It is of special moment that only a few drops of 
blood (i to 10) be introduced into a tube containing 10 c.c. of 
culture-medium, since the blood often contains certain proper- 
ties the result of bacterial development (agglutinins and bac- 
terial products), which, unless highly diluted (1-50 to 1-250), 




no THE BLOOD. 

interfere with the growth of the bacteria, and at times prove 
germicidal to them. Cultures from the blood should be kept 
at an incubating temperature (37.5° C.) for at least twenty- four 
hours, and in the case of the tubercle bacillus, for from ten days 
to two weeks — glycerin-agar being employed as a culture-medium. 

Collecting blood in this manner for bacteriologic study does 
not cause more pain than does the introduction of the hypodermic 
needle, and if done under thorough aseptic measures should 
not be attended by ill results. The gonococcus may be culti- 
vated in low dilution (1-2) on a medium of agar and blood-serum; 
and special media will also be necessary in the cultivation of the 
bacillus of influenza and the Bacillus aerogenes capsulatus, for 
which the reader is referred to special works on bacteriology. 

Blood from the peripheral circulation when smeared upon 
slides or cover-glasses may show bacteria, but this finding is 
rather unusual and a negative result would be of no clinical 
moment; while a positive result, which is seldom obtained, bears 
some clinical significance. It is possible to obtain the bacillus 
of leprosy in this manner by making a puncture into the skin 
overlying one of the tubercles; and I have obtained smears show- 
ing the bacillus of leprosy within the bodies of the leukocytes, 
in blood drawn through the healthy skin (see Leprosy, page 112). 
Blood collected from near the initial wound, in tetanus, often con- 
tains the tetanus bacillus. The bacillus of anthrax is commonly 
found in this manner and, with less frequency, the Bacillus mallei. 

Films. — Smear the blood upon slides, exerting but Httle 
pressure, since a spread far too thick for ordinary study is pref- 
erable. Immerse the dried films in a 5 per cent, aqueous 
solution of acetic acid for ten seconds to remove the hemoglobin 
from the erythrocytes; dry by blowing upon the specimen, and 
then hold it, face down, over the open mouth of a bottle containing 
ammonia to neutraHze the remaining acid. 

Staining. — Staining may be accomphshed by the ordinary 
anilin dyes (carbolfuchsin, anihn-gentian-violet, etc.). Gunther 
recommended staining with the latter solution for twenty-four 
hours, then treat with 1-14 solution of nitric acid until a light- 
green color develops; wash in alcohol, dry in the air, and mount. 
The erythrocytes do not stain after treatment with acetic acid, 
and bacteria, when present, comprise a conspicuous feature of 
the specimen. 

Animal Inoculation. — It has been my practice to always 
have at hand a healthy guinea-pig for the purpose of inoculating 
with the blood obtained for bacteriologic study, and to inject 
from five to twenty minims either beneath the skin or into the 



BACTERIA OF THE BLOOD. 



Ill 



peritoneal cavity of the animal. Certain hemic changes follow 
similar injections with normal blood — loss of hemoglobin and 
leukocytosis; but bacteremia, abscess, or death of the animal 
results from the introduction of bacteria. 



BACTERIA OF THE BLOOD. 

Anthrax. — The bacillus of anthrax was first detected in the 
blood by Pollenderin 1849. The bacilh are best demonstrated in 
the blood by inoculating an animal with a virulent culture and 
studying its blood within twenty-four hours. They are always 
present in the heart's blood at postmortem, may be transmitted 
from the mother to the fetus, and have been found in the hquor 
amnii. 

Relapsing Fever. — Obermeicr in 1873 described a flexible 
spiral organism, about o.i [i 
in diameter and from 20 to 
40 [Jt in length, as occurring 
in the blood of persons suffer- 
ing from relapsing fever dur- 
ing the paroxysmal stage of 
the disease (Fig. 43). Since 
the original report of Ober- 
meier little further has been 
learned regarding this organ- 
ism. During the paroxysm 
they are generally very numer- 
ous, occurring as long, slen- 
der, and flexible spirochaeta, 
and display vigorous move- 
ments. Their extremities are 
pointed. The spirillum of 

Obermeier stains readily by the ordinary dyes (two to five min- 
utes), but not by Gram's method. Efforts to cultivate the organ- 
ism have been unsuccessful; Koch, however, is reported to have 
cultivated the spirillum, and to have demonstrated the formation 
of spores. During the interval between paroxysms there are to 
be seen small, refractile globules (coccus hke), which v. Jaksch 
believes transform into spirochaeta. After the crisis they are found 
to be motionless, and many of them have been engulfed by the 
leukocytes.* 

Albrecht has described at length an interesting series of obser- 
vations.! He collected the blood, during the afebrile period, 




Fig. 43. — Spirilla of relapsing 
blood (X 1000) 



fever in human 



* "Annal. de I'lnstitut Pasteur," iSgi, p. 545. 
t "Deut. Archiv f. klin. Med.," vol. xxix,^p. 77. 



112 THE BLOOD. 

in moist chambers, and after from five to six days many of these 
specimens became loaded with spirilla. The spirillum may be 
kept living for a long time — "one hundred and eighty days" — 
in defibrinated blood at a temperature of 20° C. It is destroyed 
by fluid from the serous sacs, urine, saHva, oxygen, and COg. 
The disease may be transmitted to both man and apes by inocu- 
lation with the blood of infected patients. 

Tubercle Bacillus. — The tubercle bacillus is to be encountered 
in the blood of acute mihary tuberculosis, and at the same time 
the bacilli may also be found in the urine without the existence 
of tuberculous lesions of the genito-urinary tract. Tubercle 
bacilli have also been found in the blood of the fetus when born 
of a tuberculous mother. It does not follow, however, that tubercle 
bacilli are at all a common finding in the blood. The various 
observers have found the blood of tuberculous persons to contain 
staphylococci and streptococci; while negative results have been 
equally numerous. The method most likely to prove satisfactory 
is the inoculation of a guinea-pig with blood from a person known 
to be tuberculous. 

Leprosy. — The Bacillus leprae may be found in the blood 
during the advanced stage of this disease, yet, generally speak- 
ing, it rarely enters the circulation. When an incision is made 
directly over a tubercle and pressure made upon this mass, 
the blood which exudes is likely to contain lepra bacilli. Stre- 
ker* found lepra bacilli in the leukocytes in all of five cases 
examined; while Brownf detected these bacilh in the polymor- 
phonuclear leukocytes in nine out of sixteen cases examined. 
In a case studied through the courtesy of Dr. John V. Shoemaker 
blood drawn from a rather deep incision through the normal 
skin of the finger was prepared in the usual manner, fixed by 
heat, and stained for the ''Bacillus leprae" with carbolfuchsin, 
and counterstained by Gabbett's methylene-blue solution. Such 
specimen smears contained few polynuclear leukocytes, in the 
protoplasm of which lepra bacilli were readily seen ; the smallest 
number of bacilh observed in a polynuclear leukocyte being two, 
and the greatest number eight. Bacilli were also found free 
in the plasma, and in this situation occurring singly or at most 
two or three in a single field (Plate 5).! Streker found extra- 
cellular bacilli in all of his cases. 

Typhoid Fever. — Bacillemia is not an uncommon concomit- 
ant of typhoid fever, though until recently typhoid bacilh were 

* "Miinchener med. Wochenschr.," 1897, p. 1103. 
t "Trans. Cal. Med. Soc," 1897, p. 168. 
j "Proc. Phila. Co. Med. Soc," Jan., 1903. 



PLATE 5. 




A g| C7CXW figj., <f 






-3 



^ r^i^ 



s^. 







The Blood-cells in Leprosy. 

1. Blood from a case of leprosy stained with eosin and hematoxylin. Note the 
numerous nucleated erythrocytes; at the right, one showing two nuclei; at the left, 
one with nucleus situated on the margin of the cell. 

2. Blood stained with carbolfuchsin and methylene-blue, and showing lepra 
bacilli (obj. Queen one-twelfth oil-immersion). 



BACTERIA OF THE BLOOD. II3 

not supposed to enter the blood. In mothers suffering from 
typhoid the bacillus of Eberth has been repeatedly isolated from 
the blood of both the fetus and the placenta. R. C. Rosenberger,. 
in an exhaustive monograph,* to which is appended a complete 
bibliography, collected from the hterature reports of 518 cases 
of typhoid fever wherein the blood was examined for the bacillus 
of Eberth, with positive results in 419 of the cases, or 80.8 per 
cent. Typhoid bacilU may be found in the blood early during 
the course of the disease. The bacillemia has not been shown 
to bear a direct relation to the occurrence of the bacillus of Eberth 
in the urine, yet were the blood and urine to be studied cori 
relatively, it is highly probable that a more or less direct relation 
would be found to exist between bacillemia and bacilluria. 

Suppuration. — The ordinary pus-producing organisms, the 
streptococcus, staphylococcus, and Bacillus pyocyaneus, have 
been isolated from the blood in cases wherein suppuration existed 
and in chronic tuberculosis. Von Eiselberg| found specific bac- 
teria in the blood of 77 out of 1 56 cases of sepsis examined. Among 
the organisms found were the streptococcus, staphylococcus, 
pneumococcus, gonococcus, and the Bacillus coH communis. 
He also isolated specific bacteria from the blood in i out of 3 
cases of puerperal sepsis. The Bacillus enteritidis, streptococcus, 
staphylococcus, and Bacillus coli communis have been found in 
the placental blood of women suffering from, apparently, local 
sepsis. An infant born of a mother suffering from facial ery- 
sipelas showed streptococcemia and ulcerative endocarditis. 
Blood withdrawn from the vein during the course of erysipelas 
is likely to be free from bacteria, but taken from the vicinity 
of the infected area it is apt to contain cocci, as has been repeatedly 
demonstrated by the author. 

Pneumonia. — During the course of croupous pneumonia 
the pneumococcus may be found in the circulating blood and in 
the fluid from infected joints. Rosenowf obtained cultures of 
the pneumococcus in 160 out of 175 bloods examined; positive 
results were obtained in all stages of the disease and in 47 out 
of 80 cases studied by blood smears. In reports of 56 examina- 
tions collected from the literature (Rosenberger) diplococci were 
found in 29 instances. Beco isolated the bacillus of Friedlander 
from a case of pneumonia due to this organism. I have isolated 
the bacillus of Friedlander from the heart's blood, meninges, car- 
diac abscess, and from the lung in a subject dead of pneumonia. 

Influenza. — Cannon recovered short bacilli from the blood 

* " The Bacteriology of the Blood," " Amer. Jour. Med. Sci., " August, 1903. 

f'Wien. klin. Wochenschr.," 1890. 

j"Jour. Amer. Med. Assoc," March 18, 1905, p. 871, 



114 THE BLOOD. 

in 20 cases of influenza, but this organism has also been obtained 
from the blood of scarlet fever, measles, chicken-pox, and diph- 
theria, which renders this finding of limited value. 

Epidemic Meningitis. — In epidemic cerebrospinal meningi- 
tis Gwyn,* among other observers, has recovered the Diplococcus 
intracellularis of Weichselbaum (Fig. 213) from the venous blood 
during Hfe. I have also obtained this organism from the heart's 
blood at postmortem, but efforts at its cultivation before the 
patient's death have been, with but a single exception, of no avail. 
In one instance I recovered a pure culture of the diplococcus of 
pneumonia from the venous blood antemortem, and from the 
cerebrospinal fluid both the pneumococcus and the Diplococcus 
intracellularis were cultivated during hfe and at postmortem. In 
another case a bacillus (colon group) was cultivated from the venous 
blood antemortem, and the colon bacillus and the Diplococcus in- 
tracellularis were recovered from the meninges at autopsy. The 
pneumococcus has been isolated from the blood of the fetus where 
the mother suffered from cerebrospinal meningitis. f 

Purpura. — Letcherich found large bacilH in the blood of 
purpura hcemorrhagica, while other observers have recovered 
cocci. In three cases studied antemortem I was unable to culti- 
vate bacteria from the venous blood. 

Ulcerative Endocarditis. — In acute ulcerative endocarditis 
the various pus-producing organisms have been cultivated from 
the blood, and in addition to these Gwynt has recovered the 
Bacillus aerogenes capsulatus. 

Gonococcus. — Johnson,^ among other observers, has culti- 
vated the gonococcus from the blood of persons suffering from 
gonorrheal endocarditis. 

Plague. — In bubonic plague bacillemia occurs, as is shown 
by Atkinson's II study of 273 cases, in 221 of which the Bacillus 
pestis was isolated from the blood (81 per cent.). Rosenberger 
has collected reports of blood examinations of 433 cases of bubonic 
plague with positive results in 300 instances (69 per cent.). 

Diphtheria. — The diphtheria bacillus may be cultivated 
from the blood in malignant forms of the disease. 

Fungi. — In connection with general furunculosis Weber** 
recovered blastomycetes from the blood. 

Malta Fever. — During the course of Malta fever the Micro- 

* "Johns Hopkins Hosp. BuL," i8gg, p. 112. 
t "Schmidt's Jahrbuch," 1893, p. 227. 
t "Johns Hopkins Hosp. BuL," 1900, p. 185. 
^ Ibid., Oct., 1902. 
II "Lancet," Jan. 26, 1901. 
** "Society of Internal Med.," Beriin, Dec, 1902. 



INVASION OF THE RED BONE-MARROW BY BACTERIA. II 5 

COCCUS melitensis may be recovered from the blood of the venous 
circulation, and when cultivated from this source will be found 
to agglutinate with the patient's serum (see page 125). 

Chorea. — Leredde obtained a pure culture of the Staphylo- 
coccus pyogenes albus from the blood of a case of chorea com- 
phcated by endocarditis. In chorea the cadaveric blood has been 
found to contain bacteria. 

Scarlet Fever. — During the course of scarlet fever Raskin* 
found a Staphylococcus pyogenes in the circulating blood in 2 
out of 64 cases examined. Class has found the diplococcus of 
scarlatina to invade the circulation; while other observers have 
conducted systematic researches which were attended with nega- 
tive results. 

Scurvy. — According to Rosenell, Murri, Muller, and Wieruszky 
bacteremia may occur during the course of scurvy, but the latter 
of these observers was unable to show any relation between the 
bacteria recovered from the blood of scorbutic patients and this 
disease. In elephantiasis, valvular heart disease, and carcinoma 
bacteria have been isolated from the blood. 

Leukemia. — The Hterature contains detailed bacteriologic 
reports of 96 cases of leukemia, 49 of which were chronic. f 
In nearly one-third of the cases bacteriologic study was nega- 
tive, and many bacteria were classified only as cocci or bacilH. 
Among the determined organisms were Streptococcus pyogenes, 
Staphylococcus citreus, aureus, and albus, pneumococcus, sar- 
cinae, bacillus of Friedlander, Bacillus proteus, and the colon 
bacillus. In 12 of the cases short, thick baciUi with rounded 
ends were found; and spore-formation was suspected or noted 
occasionally, while clear central spaces in the bacilli were re- 
peatedly mentioned. 



INVASION OF THE RED BONE-MARROW BY BACTERIA. 

E. FraenkelJ reports a series of observations upon the red 
bone-marrow during the course of the various acute infectious 
maladies. It does not always follow, from these observations, 
that the specific organism of the disease from which the patient 
is suffering is the one found to invade the bone-marrow. Second- 
ary infection of the bone-marrow during the course of acute 
febrile conditions was found to be rather common. 

* "Centralbl. f. Bakt.," 1889, p. 286. 

t Nichols, "Amer. Med.," July 18, 1903, p. 102. 

+ "Mitt. a. d. Grenzgeb. d. Med. und Chirurg.,'' v<,l. xii, p. 419. 



Il6 THE BLOOD. 

Typhoid Fever. — Fraenkel recovered typhoid bacilli from 
the bone-marrow of patiems suffering from typhoid fever during 
all stages of the disease, and makes the assertion that typhoid 
bacilli are invariably present in the bone-marrow. In this con- 
nection the reader is referred to the invasion of the blood by 
t}'phoid bacilh, page 112, since the question of bacillemia must 
of necessity cause an invasion of the bone-marrow with t}^hoid 
bacilh. Typhoid bacilli remain in the bone-marrow after the 
local lesions in the intestine are healed. 

Tuberculosis. — In chronic pulmonary tuberculosis specific 
bacteria are rarely to be recovered from the bone-marrow; nor 
is it at all common to find the organisms of secondar}- infection 
present in the marrow in this malady. 

Diphtheria. — It is extremely unusual to recover the diph- 
theria bacillus from the bone-marrow during the course of 
diphtheria, a condition readily explained through the fact that 
bacillemia is not a common feature of diphtheria. Fraenkel 
found the bone-marrow to be invaded with streptococci in many 
of the cases of diphtheria. 

Scarlet Fever. — In scarlet fever streptococci are an almost 
constant finding in the bone-marrow. There appears to be no 
constant period, during the course of the disease, at which time 
the streptococci enter the bone-marrow^; and the period during 
which they may be recovered from this situation varies greatly 
with different types of the disease. 

Erysipelas. — In er}'sipelas specific bacteria may be found 
in the bone-marrow during the acute stage of the disease. These 
organisms are to be found in large numbers after the local symp- 
toms have subsided. 

Clinical Significance. — The direct injury that the bacteria 
must exert upon the bone-marrow^ serves to explain, in a measure 
at least, the blood changes common to this and other infectious 
maladies. Infection of the bone-marrow with bacteria appeals 
to one as the possible foundation for many, and possibly all, 
the hematologic changes present in acute infectious conditions. 

The recover}^ of specific bacteria from the red bone-marrow 
does not appear to be a chnical finding w^orthy of special descrip- 
tion, since the same bacterium may be more easily cultivated 
from the blood. 

SERUM-DIAGNOSIS. 

Serum-diagnosis is based upon a study of the pathologic 
chemistry of the blood, and has been found of the utmost im- 
portance in the recognition of disease, though it is only possible 



SERUM-DIAGNOSIS. II7 

at present to detect the presence of a limited number of varieties 
of infection. The reactions that take place through serum- 
diagnosis may be conveniently classed under the following head- 
ings: 

I. The reaction between a pure culture of a micro-organism 
and the serum of an animal infected with the same organism: 
(a) The agglutination; (b) solution of the micro-organism; (c) 
formation of a tangled mass composed of motionless filaments 
of micro-organisms; (d) the production of a precipitate when 
serum of an infected animal and the filtered culture (germ-free) 
of the bacterium causing the infection are mixed. 

II. Reaction between erythrocytes of one species of animal 
and the serum of another species into w^hich the erythrocytes 
of the former animal have been injected: (a) Agglutination of 
the erythrocytes; (b) solution of the erythrocytes with the forma- 
tion of a precipitate should the serum of the animal injected 
be mixed with that of an animal of the same species as the one 
from which the blood-corpuscles were taken. Neisser and Daring 
have shown that the usual reaction between human blood -serum 
and the blood of animals of another species is curiously modified 
in uremia. Human serum (active) yV c.c, dissolves the blood- 
cells in I c.c. of rabbit's blood, and the fluid becomes clear in 
two hours. After the thermolabile complement of the serum is 
destroyed by heat and a quantity of it mixed with the native 
serum, the addition of the rabbit's blood will not affect the usual 
reaction, but the fluid remains cloudy and the corpuscles are 
not dissolved. 

Streptocolysis. — It has been shown by various observers, and 
more recently by G. F. Ruediger,* that virulent streptococci 
when grown in heated rabbit's serum and other serums develop 
a hemolysin which is capable of destroying the erythrocytes of 
several animals. This product (hemolysin) is an organic sub- 
stance which is destroyed by a temperature of 70° C. for two 
hours; deteriorates at incubating and room temperatures; but 
may be kept for a longer period in a refrigerator; is non-dialyz- 
able, and is destroyed by peptic digestion. 

Streptocolysin is composed of a haptophore and a toxiphore 
group which appear to be rather firmly united. Chickens' 
serums are capable of neutralizing the haptophore group; while 
the toxiphore group is destroyed by zinc chlorid. The red cells 
of man and of the rabbit are least resistant. The cells of the 
chicken, ox, and horse are hastened to dissolution by first washing 
them in normal salt solution. 

* "Jour. Amer. Med. Ass.," Oct. 17, 1903. 



Il8 THE BLOOD. 

The serums of certain animals have an antistreptocolysin. 
Formaldehyd in weak solution exercises an antihemolytic power. 
The filtered culture of a virulent streptococcus in heated serum 
will be found toxic for rabbits. 

III. Reaction between normal blood-serum and bacteria, 
which consists in both agglutination and solution. 

IV. Reaction between a pure culture of one class of bacteria 
and the erythrocytes. 

V. Reactions between both normal and pathologic serums of 
animals and the blood-corpuscles of animals of the same or of 
other species, which consist of solution and agglutination. 

VI. A reaction occurs between the serum of one species of 
animal and an emulsion of cells derived from the organs of another 
species, the animal having been previously injected with the 
emulsion, and consists in solution, except when the cells are motile 
(spermatozoa), when agglutination occurs. There is a reaction 
which also takes place within the body after active serums derived 
from inoculated animals or from normal animals of certain species 
are injected experimentally. This change is termed hemolysis, 
and simulates that found in pernicious anemia. 

VII. Halban and Landsteiner * have recently shown that the 
serum of maternal blood is far more active than is that of fetal 
blood — viz., {a) It requires a larger number of corpuscles to un- 
dergo solution; (6) agglutinates blood-corpuscles more actively; 
(c) has a stronger action against bacteria and against the process 
of fermentation; and {d) is more potent as an antitoxin and 
against immunizing serum. This explains the readiness with 
w^hich the new-born are infected. A point of practical importance 
is to ascertain at what period of extra-uterine life infantile serums 
become active. The specific agglutinin results in the precipi- 
tation of all bodies suspended in the media. Non-specific ag- 
glutinin is associated with a precipitate of the motile bodies only, 
the bacteria remaining passive. The hanging-drop method may 
be apphed in the study of hemoprecipitins.f 

WIDAL REACTION. 

Most characteristic and valuable among the reactions for 
serum-diagnosis is that of the Widal reaction, which is usually 
referred to in connection with typhoid fever, but the same technic 
employed in this reaction, with slight deviation, serves as a basis 
for the various other serum reactions. 

Method. — Collecting of the Blood. — Two methods are in 

* Anatomical Institute, Vienna. 

t Robin, "Phila. Med. Jour./' Dec. 20, 1902, p. 1019. 



WIDAL REACTION. 



119 



A^- 



\ 



D- 



vogue for collecting the blood for the Widal reaction: (a) The 
dry method, in which a piece of glazed paper 
is allowed to touch the summit of a drop of 
blood, and is dried in the air; (b) by collect- 
ing the blood in the capillary pipet and dilut- 
ing. Wright has suggested a special pipet for 
collecting the blood (Fig. 44), and Widal has 
found that even a less complicated pipet serves 
well for this purpose, (i) Draw the blood into 
the pipet ; heat the extremities to seal them off, 
after which the pipet and its contents are con- 
veyed to the laboratory. (2) After sufficient 
time has elapsed for the serum to separate 
from the clot, break off the ends of the pipet 
and expel the serum into a sterile watch-glass 
(labeled). (3) By means of a graduated pipet, 
transfer a portion of the serum to another 
watch-glass containing saline solution. In this 
manner dilutions 1-20, i-ioo, 1-500 or more 
are readily accompHshed. Wright's tubes are 
easily made from the glass tubing always at 
hand in the laboratory. 

Culture. — A pure culture of typhoid bacilli 
is transferred to a series of agar slants, mak- 
ing one or more cultures each day. Place in 
the dark at room temperature, and when the 
culture is from ten to fourteen days old, trans- 
fer it to bouillon and allow the second culture 
(bouillon) to remain at room temperature for 
twenty-four hours. By this method the typhoid 
bacilli develop to a large size, and their move- 
ments are rather sluggish when studied correla- 
tively with bacilH grown at incubating tempera- 
ture (37° C), and spontaneous clumping is 
rarely seen. I have employed this method 
during the past six years and have had no 
reason to modify it in any way. It is the 
method now in use by the Board of Health 
of Philadelphia, and its perfection is due to 
the careful work of Dr. Stewart, Director of 
that department. 

I. When the blood has been collected upon 
glazed paper, add 20 to 40 times its quantity 
of sterile bouillon to the drop, when make 



. B- 



A- 



Fig. 44. — Wright's 
pipet (actual size) : A, 
Open end of capillar>' 
tube; B, index; C, mix- 
ing chamber; D, con- 
necting capillary tube ; 
E, air-chamber ; F, 
sealed end. 



I20 THE BLOOD. 

gentle friction with a platinum loop over the surface of the drop 
at its margin, thereby assisting in its solution and the mixing of 
the serum with the bouillon. In this way an approximate dilu- 
tion of I-20 or greater is obtained. 

II. Place a drop of the mixture (blood and bouillon) upon 
the center of a cover-glass, and to it add a small drop of the 
twenty-four-hour bouillon culture of typhoid bacilH; mix gently. 

III. Place a ring of vaselin just beyond the margin of the 
excavation on a hanging-drop slide (Fig. 45), and then invert 
the shde over the cover-glass, taking care that the drop of hquid 
upon the cover-glass corresponds to the center of the excavation 
upon the shde. Press the shde firmly upon the cover-glass to 
which it adheres. Invert the shde quickly and the specimen 
is now ready for examination under the microscope. 

Caution. — Should too much vasehn be employed or the shde 
be turned slowly or should the drop of hquid be too large, the 
fluid will collect around the margin of the excavation. Properly 
prepared, the drop occupies the center of the cover-glass sus- 
pended from its under sur- 
face into the chamber of 
the slide. When the blood 

Fig. 45. —Lateral view of a hanging-drop slide, ^^'^ been COlleCtcd m the 

cover-glass in position. pipet, break the extremities 

of the tube and force out 4 
or 5 drops of the serum by blowing; then place a small drop 
upon the center of the cover-glass, add salt solution or bouillon 
to effect the dilution, and follow by adding a drop of the typhoid 
culture, and proceed as previously outlined. Place the specimen 
upon the microscope under a one-fifth or, better, a one-sixth ob- 
jective, and adjust the mirror, condenser, and iris diaphragm so as 
to permit of a moderate amount of hght. 

To reiterate, a one-sixth objective focuses at a point just suf- 
ficiently distant above the cover-glass to enable one to see between 
the cover-glass and the tip of the lens when the eye is brought on 
a plane with the table of the microscope. A common source of 
annoyance is the breaking of the cover-glass by the objective. 
Place the eye in position and elevate the objective gradually, when 
the motile bacteria come into view. Should there be no evidence 
of a reaction, actively motile bacilli are seen equally disseminated 
throughout the field. 

The Reaction. — The various steps in the reaction may be 
classified as follows: (a) Place the center of the drop of liquid 
under the objective, and actively motile bacilli will be seen through- 
out the entire field, {h) The first evidence of a reaction is de- 



WIDAL REACTION. 



121 



tected by retarding movements of the bacilli, (c) A small bacillus 
attaches itself to the side of a larger organism, — the Y formation, 
— and later other bacilli are seen to come in contact with these; 
some of them remaining to form a clump, while others by active 
movements detach themselves from the clump and again appear 
free in the liquid. As the movements of the bacilli lessen, more 
and more bacilli become attached (Y formation), until there 
are decided aggregations of bacilli in certain areas throughout 
the entire drop of Hquid (Fig. 46) . (d) The reaction is not complete 
until all motihty of the organisms composing these various aggrega- 
tions has ceased. 

Caution. — Clumping may be found at the margin of the drop 




Fig. 46. — Positive Widal reaction; dilution 1-40 (obj. B. and L. one-sixth). 



when the test is made with normal blood; therefore only central 
clumping is of cHnical value. 

Methods of Making Records. — Number each shde and place 
under the microscope as soon as they are prepared. Note carefully 
which, if any, of the above-described conditions are present. Should 
there be no attempt even at Y formation or clumping, we mark 
with a wax pencil thus, — (minus), upon the right-hand end 
of the slide; but in case shght evidence of clumping is present, 
it is marked — ?; or in case there be present a feeble reaction, 
agglutination without loss of motion, it is marked -f ? (plus). 
Specimens should be examined every fifteen minutes for a period 
of one hour, at which time the last marking will be either + or — . 



122 THE BLOOD. 

It has been my rule to regard all questionable reactions as being 
negative, and to mark them — , believing it of less serious moment 
to err upon this side. 

Clinical Significance. — The Widal reaction occurs at some 
time during the course of typhoid fever in from 95 to 98 per cent, 
of all cases. The reaction cannot be said to be pathognomonic 
of this disease, since, rarely, it occurs in other febrile conditions 
and in jaundice. I have observed the reaction once in the blood 
of scarlet fever, and again in diphtheria. The reaction may 
occur early during the course of typhoid fever, but as a rule it 
is found from the fifth to the ninth day. It may, however, not 
appear until the twentieth day, or even later when convalescence 
is well estabhshed. The blood of persons who have had typhoid 
fever may give the reaction for months or years after all other 
appreciable symptoms of the disease have disappeared. I have 
obtained a decided reaction — dilution 1-40 — thirteen years after 
an attack of typhoid fever; but other observers have found it to 
persist over a much longer period. The frequency with which 
patients are told they have typhoid fever where the condition 
merely simulates this disease leaves ample room for question 
whether or not such persons have suffered a mild attack of typhoid 
at a more recent date. In my own experience I have always 
questioned the statement of the patient that he had typhoid fever 
before when the blood gave the Widal reaction three years after 
typhoid fever. The Widal reaction serves not only in distinguish- 
ing typhoid fever from other types of infection, but also in detect- 
ing the existence of typhoid infection when it develops co- exist- 
ent with some other disease. 

In the study of a series of 456 cases of suspected typhoid 
fever in the Philadelphia, the Howard, the Pennsylvania Hos- 
pitals, and from private practice the blood was collected upon 
glazed paper and the dilution approximated 1-40. A specimen 
collected at the same time and in the same manner was forwarded 
to the Philadelphia Board of Health for examination. These 
examinations were made by Dr. A. H. Stewart, who had no 
knowledge of the fact that I, too, was testing the same blood. 
Of the 456 cases, 348 were regarded by the cHnicians as typhoid 
fever, and in 341 of these both Dr. Stewart, at the Board of Health, 
and myself obtained positive Widal reactions. In the seven 
questionable cases the Board of Health had marked three of them 
as giving a doubtful reaction, and I had regarded five of them 
as giving feeble reactions. Whenever the reaction was positive, 
the chnical course was that of typhoid fever. Such chnical 
results show the Widal reaction, as practised by the Philadelphia 



WIDAL REACTION. I 23 

Board of Health, to be of great importance in the diagnosis of 
typhoid fever, since of the 456 cases examined but a single speci- 
men was received from any given case. I am not cognizant of 
such another test of the efficiency of the Widal reaction. 

Absence of the Widal reaction in typhoid fever tends toward 
an unfavorable prognosis, since in non- fatal infection an increase 
in quantity of agglutinin is to be observed early; therefore ag- 
glutination should probably be regarded as significant of a suc- 
cessful step toward protection against the disease. The reaction 
may \a.ry within wide limitations from day to day. The strength 
of the dilution, the source of the culture employed in the test, 
and the temperature at which the bacteria have been grown 
contribute Hberally toward variations in the reaction. 

Peculiarities. — Cultures from bile-stained exudates or secre- 
tions are hable to display a sHght tendency toward agglutination, 
and the typhoid bacilh are rendered non-agglutinable after expos- 
ure for two hours in immune serum that has been deprived of its 
agglutinative faculty by heating at 75° C. A series of experi- 
mental inoculations upon animals is capable of lessening the agglu- 
tinative properties of their blood. Agglutination may occur with 
the blood of infants born of mothers infected with typhoid fever; 
and rarely, in high dilution, with the blood of healthy adults. 

Body Fluids. — Agglutination may take place in connection 
with such other body fluids as the serum from bHsters, pus, 
exudate from the serous membranes (pleura, pericardium, and 
synovial sacs), but in these it is not constantly present in a high 
degree. With the urine of typhoid patients the reaction is usually 
feeble, may be present from day to day, or may disappear sud- 
denly to again reappear. Clumping is most Hkely to occur when 
the urine is employed in high dilution, and the urine of non- 
infected persons has been known to agglutinate typhoid baciUi. 
Therefore the reaction with the urine is valueless. The stools 
of typhoid patients and the milk of both typhoid patients and of 
animals inoculated experimentally with typhoid bacilli possess 
the power of agglutination. Passing milk through a porcelain 
filter deprives it of its clumping powers, as does also a temperature 
of 120° C. The cerebrospinal fluid (in low dilution, i or 3- 
10), tears, seminal fluid, bile, sahva, and the sweat all possess 
the agglutinating faculty. Weak solutions of safranin and of 
vesuvin also agglutinate typhoid bacilli. 

Inhibition. — Removal of the salts from the serum by dialysis 
prevents agglutination, and partial extraction of salts inhibits 
it. It is not thoroughly understood in what manner agglutina- 
tion takes place. 



124 THE BLOOD. 

There appears to be some question as to whether or not the 
colon bacillus is agglutinated. Sufficient tangible evidence exists, 
however, to show that colon bacilli obtained from a variety of 
sources are agglutinated when placed in typhoid serums; and 
that the blood of animals immunized to these bacilh agglutinate 
typhoid bacilH.* For description of Ficker's reaction see p. 525. 

Paratyphoid Fever. — Other micro-organisms belonging to 
the colon group, as the Bacillus mesentericus and Bacillus febris 
gastrica, have been obtained from persons who appeared to be 
suffering from atypical typhoid fever. They resembled the so- 
called paratyphoid bacillus, and were found capable of reacting 
with the blood of patients suffering from paratyphoid.f 

The bacilli cultivated from the patient's blood (venous) 
during the course of paratyphoid fever are agglutinated by the 
blood of the same individual when in high dilution (1-200, Hume; 
and i-iooo, Brion and Kayser); and by the blood of other per- 
sons who are suffering from a like infection. Such bloods do 
not agglutinate typhoid bacilli even in low dilution. The reaction 
induced by paratyphoid blood resembles that described under 
the Widal reaction for typhoid fever. J 

Dysentery. — The Bacillus dysentericus (Shiga) reacts with 
the blood of persons suffering from epidemic dysentery, but 
there do not appear sufficient convincing reports to enable one 
to estimate its clinical value. 

The work of certain foreign observers and that of Flexner, 
of New York, has placed this reaction upon a basis where it bids 
fair to contribute liberally toward both diagnosis and therapy 
in the disease. 

Plague. — Agglutination of the plague bacillus with the serum 
of persons sufifering from this infection has proved of great value 
in diagnosis. A difficulty in the reaction is that cultures of the 
plague bacillus are liable to display a mild degree of spontaneous 
agglutination. The bacilli should be emulsified with a solution 
of sodium chlorid, and the dilution from 2-1 or 20-1. Serum 
from convalescents loses its lysogenic action by age, exposure to 
light, and when heated at 56° C. for a few minutes. § 

Cholera. — A rather decided reaction is to be displayed be- 
tween the vibrio of cholera and the serums of infected persons. 
This reaction has been observed with the serums of persons 
suffering from cholitis. A positive reaction may be obtained 

* Lommel, "Miinchener med. Wochenschr.," 1902, p. 314. 
t Brion and Kayser, ibid., 1902, p. 611. 
J "Jour. Amer. Med. Ass.," Aug., 1902, pp. 187-217. 
^ Row, " Brit. Med. Jour.," May 9, 1903. 



WIDAL REACTION. I 25 

with the filtrate of a forty-eight-hour cukure, and agglutination 
is said to take place when the organisms agglutinated display a 
lessened virulence. It is also produced by such chemic sub- 
stances as formalin, safranin, and mercuric chlorid. 

Tuberculosis. — Arloing and Courmont, working with an 
emulsion of a special culture of tubercle bacilli (four weeks old), 
introduced the culture into the serum of tuberculous persons 
and animals in dilutions of 1-5, i-io, and 1-20.* 

Twenty-four hours are required for this reaction, and control 
tubes are necessary. The reaction is present in about 90 per 
cent, of all cases of tuberculosis; but since it occurs with the 
blood of 25 per cent, of all healthy persons as well as in non-tuber- 
culous conditions, its clinical value is shght. Tuberculous serum 
is also capable of agglutinating other bacteria. 

Malta Fever. — The serum of persons suffering from Malta 
fever gives a rather typical reaction with the Micrococcus melitensis 
when in high dilution (1-50 or greater). 

Glanders. — Agglutination of the bacillus of glanders with 
the serum of infected animals is a fairly constant finding. Charac- 
teristic clumping is seen in dilutions of from 1-800 to 1-400. 

Pneumonia. — Serum of persons suffering from pneumonia 
is capable of causing a rather characteristic reaction with a recent 
culture of the pneumococcus obtained from one ill of pneumonia 
or from infected animals. 

Place the serum in sterile tubes and introduce an equal quan- 
tity of a pure culture of the pneumococcus. Incubate at 37° C. 
for sixteen hours. The reaction consists in the agglutination 
of the organisms, when they sink to the bottom of the tube. Ag- 
glutination becomes more marked with the approach of the 
crisis and the previously agglutinated diplococci display a dis- 
tinct capsule. 

Bacillus Pyocyaneus. — The serum of immune animals 
is capable of agglutinating the Bacillus pyocyaneus, dilution 
1-50. The serum of animals infected with the Bacillus proteus vul- 
garis will be found to agglutinate this organism. 

Fungi. — It has been shown that the blastomycetes are ag- 
glutinated by human serum when in a very high dilution — 1-5000 
or more, — but it has not been shown that the individual yeast cells 
are destroyed by this process. f 

The precipitates induced by the addition of immune serums 
to a filtrate of bouillon culture suggest a possible aid to clinical 

*"Compt. rend, de I'Acad. des Sci.," Sept. 19, 1898; also "Gazette des 
Hopitaux," 1900, p. 137. 

t MacFadyean, "Centralbl. f. Bakt.," 1901, vol. xxx, p. 368. 



126 THE BLOOD. 

diagnosis. Typhoid bacilli are rendered inagglutinable by dis- 
solution of their capsular envelops. Agglutinin is the term appHed 
to the substance or substances by which agglutination is effected, 
but its exact nature is not known. 



SPECIAL PATHOLOGY OF THE BLOOD, 

PERNICIOUS ANEMIA. 

Among various pathologic alterations manifest in the blood 
of this condition the following occupy prominent positions: 

The oxygen capacity of the blood is commonly reduced to 
50 per cent, of the normal, or less. The hemoglobin is always 
found to be greatly reduced — 40 to 10 per cent. — during the pro- 
cess of blood destruction (active stage), but at the intervals be- 
tween the attacks the hemoglobin may rise to 50, 65, or 75 per 
cent., and may remain high for a long period. The specific 
gravity is low. Each individual erythrocyte is overcharged with 
hemoglobin {e. g., 1,000,000 red cells and 35 per cent, of hemo- 
globin — a color-index of 1.75 — 1,000,000 : 5,000,000 :: 35 : :x:, and 
X = 1.75; 5,000,000 = the normal number of red cells for 
100 per cent, of hemoglobin), although a high color-index has 
also been observed in leprosy and leukemia. During the stage 
of remission the color-index is lowered, and with the approach- 
ing relapse it increases progressively. Exceptionally, I have 
seen the color-index remain high throughout the stage of remis- 
sion, and according to some observers it may exceed that of 
the active stage. 

Significance. — A high color-index should probably be re- 
garded of bad prognostic value, while a low index and an average 
decrease in the diameter of the erythrocytes to that of the normal 
are usually observed during the dechne of the active stage, and 
may continue during the greater part of the intermission. The 
red cells increase rapidly from 1,000,000 to 2,000,000 (active 
stage) to 3,000,000 to 4,000,000, or more. The hemoglobin may 
be equally distributed among the cells (see Degeneration, page 
88) ; and the microcytes are charged with hemoglobin beyond 
their normal capacity, while the amount of hemoglobin occu- 
pying the larger cells may not be in excess when taken in corre- 
lation with their increased diameters. 

Active Stage. — Between 50 and 75 per cent, of the erythro- 
cytes show diameters decidedly above that of the normal red cell. 
The presence of microcytes often reduces the average cell-diameter 
to nearly that of the normal, and there is often a tendency for 



PLATE 6. 






'ilVM'o 



.y 



Blood of Pernicious Anemia. 

I, Normoblast; 2, megaloblasts, one showing two nuclei; 3, macrocyte; 
4, microcyte; 5, poikilocytes ; 6, ruptured eosinophiles; 7, polymorphonuclear 
leukocytes (specimen stained with eosin and hematoxylin Obj. Spencer one- 
twelfth oil-immersion). 






^6'.'"^ (?0 




Mll^oiiuf 



Blood of Chlorosis. 



I, Normal-sized erythrocyte stained deeply; 2, poikilocyte; 3, crenated erythro- 
cyte; 4, normal cells stained feebly. Note basophilic leukocyte in left half of 
plate.^ All red cells stain less deeply than do the corresponding'cells in pernicious 
anemia. (Specimen is stained with eosin-hematoxylin and methylene-blue. Obj. 
Spencer one-twelfth oil-immersion). 



CHLOROSIS. 127 

the cells to become oval or elliptic in outline (Plate 6). Poikilo- 
cytosis is marked, and many of the necrobiotic changes (polychro- 
matophiHa, etc.) described on page 91 are to be found in the 
stained specimens. 

Nucleated Red Cells. — Nucleated red cells are commonly 
found. Megaloblasts appear to bear more significance in perni- 
cious anemia than when found in the anemia of intestinal para- 
sites or elsewhere. Normoblasts and microblasts are common 
findings, and I have found the number of nucleated red cells 
per cubic millimeter to vary from 2 to 950. Cabot, however, 
has found 7000 nucleated erythrocytes per cubic millimeter. 

During the active stage leukopenia is a common occurrence. 
The decrease in the number of leukocytes concerns mostly the 
polymorphonuclear cells, and to this reduction there is a corre- 
sponding increase in the percentage of lymphocytes (30 to 70 
per cent.), yet an absolute lymphocytosis does not exist. A mild 
grade of eosinophiha and from 3 to 9 per cent, of myelocytes may 
be seen. 

Remission. — During the stage of remission a moderate 
leukocytosis may exist, such increase concerning the polymor- 
phonuclear neutrophils, and coincident with it the percentage 
of lymphocytes decreases and the myelocytes disappear. Rare, 
indeed, it is to see cases of this disease wherein leukocytosis 
and splenic enlargement with a rather high percentage of myelo- 
cytes are displayed, but their percentage does not equal that of 
leukemia. 

Significance of the Blood Findings. — 

Fatal Issue Early. Protracted Course. 

1. Progressive anemia; interval of re- i. Remissions frequent and of long 

mission short or absent. duration. 

2. Color-index high. 2. Color-index slightly increased. 

3. Increase in size of red cells, tendency 3. Red cells of normal size, or many 

toward oval and elliptic forms. cells under size. 

4. Marked degenerative changes in the 4. Little degeneration present. 

erythrocytes. 

5. Megaloblasts numerous — exceed 5. Megaloblasts few. Normoblasts 

normoblasts. plentiful. 

6. Decrease in polymorphonuclear leu- 6. Percentage of polymorphonuclear 

kocytes. cells normal. 

7. Lymphocytosis present. 7. Absent. 

CHLOROSIS. 

The chlorotic type of anemia is characterized by an increase 
in the volume of blood, decided fluidity, pallor of the drop, a 
tendency toward rapid coagulation, reduction in the percentage 
of hemoglobin, and a low color-index; e. g., 3,500,000 red cells, 



128 THE BLOOD. 

40 per cent, of hemoglobin, and a color-index of 0.57. The 
red cells are shghtly undersized, pale, and Ya.ry from 3,500,000 
to 4,500,000 per cubic milUmeter and rarely they fall to 2,000,000. 
The stained blood is less apt to show disseminated areas of pallor, 
polychromatophiha, and punctate basophiha than is the blood of 
either pernicious anemia or of grave secondary anemia (Plate 6), 
but poikilocytosis is Avell marked. Normoblasts are encountered, 
and the blood-plates usually increased. Leukocytosis is absent 
in uncomplicated cases, while there is apt to be an absolute re- 
duction in the polymorphonuclear cells. ^Moderate lympho- 
cytosis (30 to 50 per cent.) occurs, wherein either the large or 
small lymphocytes may predominate. Eosinophilia is a rare 
symptom, and myelocytes have been observed. 

Hydremia. — According to the view of Smith, the volume 
of blood may be one-half or more greater than that of normal, 
and there is an absolute increase in the number of both red and 
white cells, but such increases are masked by the excess of plasma. 
Smith further beheves that treatment decreases the plasma, and 
thus restores the normal condition. These views, however, are 
not universally accepted. 

Specific Gravity. — The specific gravity is in direct cor- 
relation to the hemoglobin, and its estimation is often of the 
utmost clinical value, since it may fall to 1.025 to 1.035 (^-^SQ ^^ 
1.060 normal). 

Nucleated Erythrocytes. — Normoblasts are occasionally de- 
tected in chlorotic blood, and their number increases with the 
severity of the condition. 

• During convalescence the red cells are increased, and later 
the coloring-matter and specific gravity return to normal. Sec- 
ondary anemia without leukocytosis may be indistinguishable from 
chlorosis. 



TABLE DISTIXGUISHIXG HEMATOLOGIC FEATURES BETWEEN 

PERNICIOUS ANEMIA, CHLOROSIS, AND SECONDARY 

ANEMIA. 

Perxicious Anemia. Chlorosis. Secondary Anemia. 

1. Disproportionate re- i. Decided reduction of i. Hemoglobin and red 
duction in the hemo- hemoglobin ; color- cells reduced propor- 
globin and red cells; index low tionately; color-index 
high color-index. about normal. 

2. Red cells may fall to 2. Usually 3,500,000 to 2. Rarely below 2,000,- 

1,000,000 per cubic 4 500,000. 000. 
millimeter or lower 
during the active 
stage. 

3. Leukocytosis absent; 3. Absent. 3. Presence or absence 
leukopenia the rule. not diagnostic. 



PLATE 7. 



& 







O^"^ 



3Vt 



o 




€a^m*U^ 



Blood of Myelogenic Leukemia. 

I, Myelocytes; 2, eosinophilic myelocytes; 3, eosinophile; 5, mast-cell; 6. 
nucleated erythrocytes, one with clover-leaf nucleus and one with nucleus on cell's 
margin (stained with Jenner's stain. Obj. B. and L. one-twelfth oil-immersion). 









LEUKEMIA. 




129 


PEENiciors Anemia. 




Chlorosis. 




Secondary Anemia. 


4- 


Lymphocytosis; poly- 


4- 


Lymphocytosis; poly- 


4- 


Increase affects most- 




nuclear cells re- 




nuclear elements de- 




ly the polynuclear 




duced. 




creased. 




cells. 


5- 


Eosinophilia absent. 


5- 


Absent. 


5- 


Present under certain 
conditions. 


6. 


iMyelocytes few. 


6. 


Extremely rare. 


6. 


Occasionally seen in 
varying numbers. 


7- 


Diameter of red cells 


7- 


Diameter decreased 


7- 


Most cells of normal 




increased; oval and 




or normal. 




size. 




elliptic forms com- 












mon. 










8. 


Erythrocytes stain 


8. 


Stain feebly — many 


8. 


Appear normal or 




deeply. 




as mere shadows. 




moderately pale. 


9- 


Megaloblasts exceed 
in number the nor- 
moblasts. 


9- 


Normoblasts few. 


9- 


Normoblasts present; 
megaloblasts rare. 


[O. 


Specific gravity low. 


ID. 


Reduction in propor- 
tion to loss of hemo- 
globin. 


ID. 


Reduced — follows 
course of hemo- 
globin. 


[I. 


Not materially al- 
tered. 


II. 


Blood - plates in- 
creased. 


II. 


J fluctuate greatly. 



DifficuUies . — It is not uncommon to meet cases wherein one 
is unable to decide hematologically to which of these three types 
of anemia the case belongs; and here the diagnosis is to be 
achieved through a comparative study of both the general chnical 
features and the blood findings. Obscure syphiHs, gastric car- 
cinoma, intestinal parasites, purpura, malaria, typhoid fever, 
and less often mineral poisons may be found to produce changes 
in the blood which closely resemble those found in pernicious 
anemia. Except in anemia of parasitic origin megaloblasts are 
seldom found. 



LEUKEMIA. 

Leukemia is a disease characterized by hyperleukocytosis, 
a proportionate reduction in both the hemoglobin and the red 
cells, the occurrence of nucleated erythrocytes, and the presence 
of myelocytes. Generally speaking, leukemia may be divided 
into two classes, myeloid and lymphoid. Myeloid blood is found 
when there exist hypertrophy of the spleen and marrow changes 
with Uttle or no involvement of the other lymphatic tissues. 
Lymphoid blood may be associated with acute or chronic forms of 
this disease, and occurs when some of the lymphatic glands are 
enlarged, though visible glandular enlargements may be absent, as 
was noted in the case from whom the blood was obtained for 
Plate 9. There may be enlargement of the spleen. Both types 
of the disease (mixed leukemia) may exist in the same individual. 
Leukemia is one of the few conditions wherein we are able to 
make a diagnosis from the hematologic findings alone. 
9 



I30 



THE BLOOD. 



MYELOID LEUKEMIA. 

The blood exudes slowly from the puncture, is opaque, may 
resemble thin pus, and spreads upon sHdes with ditlicuhy. The 
fibrin and the time for coagulation are about normal. 

Red Cells. — During the early stage the red cells are nearly 
normal in number, but with the advance of the disease they are 
reduced to from 3,500,000 to 2,000,000 or less. I have seen the 
red cells remain near the normal point until late in the disease. 
The hemoglobin is also reduced, giving a color-index of from 
0.5 to 0.6. Nucleated red cells are to be found in great numbers 
independent of the degree of anemia, varying as they do from 
5000 to 50,000 or more per cubic milhmeter. The majority of 
these cells are normoblasts, and many show fragmentation and 
mitosis of their nuclei (Fig. 47). Other changes in the red cells 
common to grave anemia are also prominent in myeloid blood. 
Polychromatophihc erythroblasts are commonly seen (Plate 8) and 




Fig. 47. — I, Mitosis of red corpuscle from leukemic blood ; 2, myelocyte from same blood ; 
3, megaloblast from case of fatal anemia ; 4, myelocyte from leukemic blood (after George 
Dock '• . 

were present in all of ib cases that have come under my observa- 
tion. 

White Cells. — At first the white cells may vary from 60,000 
to 100,000 per cubic milhmeter, but later they are found to num- 
ber about 400,000 to 500,000, and may reach 1,000,000 per cubic 
milhmeter. Correlatively speaking, the leukocytes and red 
cells may be found i : 100, i : 50, or even 1:10, tluctuating during 
different hours of the day. The fresh blood is found to contain 
many leukocytes, some of which show ameboid movement (myelo- 
cyte). In one instance (personal observation') with a leukocyte 
count of 550,000 per cubic millimeter and 34 per cent, of myelo- 
cytes all symptoms were modified and the leukocyte coimt fell 
within a period of six weeks to 25,000, myelocytes disappeared, 
and the patient was reported by another observer as cured. Cabot 
cites a similar instance. As a rule, however, during the stage of 
remission the percentage of myelocytes remains high. 



PLATE 8. 









bo o 

















C 



1 



1 













^ 



Blood of Splenomedullary Leukemia. 

I, Myelocytes; 2, eosinophilic myelocyte; 3, leukocytic shadows; 4, poly- 
chromatophihc megaloblast ; 5, large mononuclear leukocyte; 6, small lympho- 
cyte; 7, eosinophile; 8, megaloblast; 9, polymorphonuclear leukocyte; 10, small 
eosinophiles (stained with eosin and hematoxylin. Obj. B. and L. one-twelfth 
oil-immersion). 



LYMPHATIC LEUKEMIA. I3I 

Myelocytes. — The distinguishing feature of myeloid blood 
is the high percentage of myelocytes present — 20 to 60 per cent. 
(Plate 8) (see Myelocytes, page 97). There is an absolute increase 
in the number of polynuclear cells, though their percentage upon 
differential count is somewhat reduced. They are seen to vary 
within wide hmits as to size, staining properties, and peculiarities 
of their nuclei, which constitute an important feature in leukemic 
blood (dwarfed cells, giant cells, cells containing coarse granules). 
Border-hne cells between the myelocyte and the polynuclear 
leukocyte are frequently encountered; Cabot prefers to classify 
such cells as transitional neutrophils. The lymphocytes usually 
occupy from 20 to 30 per cent, of the total number of leukocytes, 
but they, too, show an absolute increase, and the percentage 
of large and small forms varies greatly in different cases. Large 
lymphocytes which stain not unlike myelocytes are often seen; 
and cells, apparently small lymphocytes, display granules. 

The eosinophils show an absolute increase and their percent- 
age may var}^ from i to 15 or more. In leukemia there are to be 
distinguished polynuclear eosinophils of normal size, eosinophilic 
giant cells often containing coarse granules, dwarfed eosinophils, 
and the eosinophihc myelocyte (see Plate 8). Eosinophils at 
times contain basophilic granules. 

Basophils. — Blood stained with thionin shows neutrophils with 
coarse granules (Mastzellen). Such cells may comprise 10 per cent. 
of the leukocytes (Plate 7). Charcot-Leyden crystals are to be found 
in myeloid blood and in blood containing many eosinophilic cells. 

LYMPHATIC LEUKEMIA. 

Lymphoid blood is characterized by ^ large percentage of 
lymphocytes (70 to 93). This form of leukemia is commonly 
acute, yet it may run a protracted course. In three cases that 
have come under my observation the leukocyte counts have 
varied from 30,000 to 450,000 per cubic millimeter, yet a higher 
degree of leukocytosis may be observed, and the red cells vary 
from 3,500,000 to 1,200,000 per cubic milhmeter. Nucleated 
red cells are less commonly met with in this condition than in 
myelogenous leukemia. McCrea, in the study of 11 cases oc- 
curring in infants, did not find nucleated red cells in the blood of 
7 of them; but in acute cases nucleated red cells are occasionally 
numerous, and were present in all of my cases. Degenerative 
changes in the red cells are fairly pronounced. The ratio of 
white to red cells has been seen to equal i : 50 or less. The large 
percentage of lymphocytes may be composed either of the small 
forms, the large forms, or of both. In one of my cases there was 



132 



THE BLOOD. 



such a gradation in the cells as to make it impossible to distin- 
guish between the large and small lymphocytes (Plate 9). In 
acute cases the large cells often predominate; such cells stain 
faintly and show evidence of degeneration, and occasionally stain 
a pinkish color. In specimens displaying mostly small lympho- 
cytes these cells stain deeply (Plate 9). 



CHARACTERISTIC 
Myelogenic Leukemia. 

1. Red cells moderately 

reduced — 3,000,000. 

2. Nucleated red cells, 

including megalo- 
blasts, numerous. 

3. Leukocytes 150,000 to 

500,000 or more per 
cubic millimeter. 

4. Myelocytes 30 per 

cent, or more. 

5. Eosinophils common, 

also eosinophilic 

myelocytes. 
'6. Neutrophils commonly 

seen. 
7. Lymphocytes — large 

and small — 20 to 

30 per cent. 



DIFFERENCES IN LEUKEMIC BLOOD 

Chronic Lymphatic 

Leukemia. 
I . Moderate reduction- 



2,000,000 to 3,000, 
000. 
Rare. 



3. 100,000 to 300,000. 

4. Myelocytes few. 

5. Eosinophils few 

6. Less common. 



Acute Lymphatic 
Leukemia. 

1. More marked reduc- 

tion early during 
course of malady. 

2. Normoblasts rather 

common. 

3. 30,000 to 200,000. 



4. Myelocytes few. 

5. Eosinophils rarely 

found. 



6. Scanty. 



7. Small lymphocytes 70 7. Lymphocytosis — large 
to 90 per cent. forms predominant. 



PSEUDOLEUKEMIA (Hodgkin^s Disease). 

Pseudoleukemia is distinguished from true leukemia through 
hematologic research only. Early during the course of this 
disease the red cells are practically normal, and with its progress 
the hemoglobin falls gradually (75 to 30 per cent.), and is soon 
followed by a reduction of the red cells. Should these changes 
develop rapidly they are accompanied by the general features 
of grave secondary anemia. The leukocytes may vary from 
5000 to 60,000 per cubic millimeter, and may increase to a ratio 
of 1 : 50 or even i : 80 of the red cells, the polynuclear cells alone 
being increased. In cases where the leukocyte count is low 
lymphocytosis is often found. EosinophiHa is seldom seen and 
these cells are usually decreased when leukocytosis exists. Similar 
blood changes are to be found in glandular tuberculosis, mahg- 
nancy, and syphilis. 

SPLENIC ANEMIA. 

A condition characterized by splenic enlargement and leu- 
kopenia. The red cells are usually between 2,000,000 and 4,000,- 



PLATE 




O Q O 



Blood of Lymphatic Leukemia. 

I, Small lymphocytes; 2, large lymphocytes; 3, degenerated lymphocytes; 4, 
polymorphonuclear leukocytes; 5, megaloblast showing fragmentation of nucleus 
and polychromatophilia of protoplasm; 6, nucleated red cells (megaloblasts); 7, 
macrocytes; 8, poikilocyte; 9, erythrocytes of normal size; o, microcyte (stained 
with eosinand hematoxylin. Obj. Spencer one-twelfth oil-immersion). 



ACUTE INFECTIOUS DISEASES. 1 33 

ooo per cubic millimeter. White cells may fall to 700; while the 
hemoglobin fluctuates between 20 and 50 per cent. Myelocytes 
and normoblasts are scanty, and moderate lymphocytosis the rule. 



ACUTE INFECTIOUS DISEASES. 

The blood changes common to infectious fevers, as the re- 
sult of temperature alone, have been alluded to (p. 108). 

Pneumonia. — Coagulation is rapid, except in cases where 
leukopenia exists. Variations in the specific gravity and poly- 
cythemia result from cyanosis. In children the specific gravity 
may be high.* The toxicity of the blood is increased, and after 
the crisis both hemoglobin and red cells are reduced. Normoblasts 
and megaloblasts may be found. 

Leukocytosis develops with the onset and persists, decHning 
with the approach of the true crisis. The polymorphonuclear 
leukocytes are both absolutely and relatively increased (90 per 
cent.), and the lymphocytes are reduced, as are also the eosino- 
phils, before the crisis; but later they are increased. Myelocytes 
and transitional neutrophils are common. The blood-plates 
are increased following the crisis. When leukocytosis continues 
after the crisis, resolution is retarded, and such compHcations 
as empyema, abscess, and gangrene cause a further increase. 
Children show high leukocyte counts. 

Significance. — Shght leukocytosis — mild infection. High leu- 
kocytosis — moderate or severe infection. Absence of leuko- 
cytosis — severe infection. In 16 fatal cases Rosenowf found the 
leukocytes to average 12,000; while 40 cases of recovery gave an 
average of 20,000. 

Typhoid Fever. — During the course of this disease the blood 
findings may vary greatly, dependent upon the existence of pro- 
fuse diarrhea, constipation, pyrexia, hemorrhage, peritonitis, 
pneumonia, etc. (see Bacteriology of the Blood and Widal Reaction), 
Blood-plates and fibrin are commonly reduced — a great reduc- 
tion being of rather bad prognosis. Leukocytosis is not a feature 
of typhoid fever, the average being about 5000 per cubic milli- 
meter, and leukopenia at times progresses with the advancing stages 
of the disease. Leukocytosis may or may not follow hemorrhage 
from the bowels, and is Hable to develop with compHcations, as 
well as when the ulceration of the bowel is sufficiently deep to 
produce local peritonitis. Thayer gives the following table show- 
ing the percentage of leukocytes found by differential counts: 

* Monti and Berggrund, " Arch. f. Kinderheilk.," vol. xvii. 
t"Jour. Amer. Med. Assoc," March i8, 1905, p. 872. 



134 



THE BLOOD. 



First week of fever 

Second " 

Third 

Fourth " 

Fifth 

Sixth 

First week apyrexia 

Second " " 

Third 



Counts. 


Polymor- 
phonu- 
clear 


Small 
Mono- 


Large 
Mono- 


Neutro - 

PHILS. 

Per Cent. 


nuclear. 
Per Cent. 


nuclear. 
Per Cent. 


12 


74 


13 


12 


39 
34 


71 
66 


14 

21 


13 1 

II ! 


19 

8 


65 
62 


20 
18 


14 
19 


4 


58 


22 


13 


12 


61 


21 


15 


7 


49 


31 


17 


' 


57 


15 


23 



Eosino- 
phils. 
Per Cent. 



0.5 
0.8 

0-3 
0.4 

0.3 
6.0 

3-0 
2-3 
3-5 



Osier* cites a case wherein the leukocytes were 5500 before 
intestinal perforation, and rose to 11,500 within fifteen minutes 
following this accident; but about three and one-half hours later 
they were found to be 7500, and six hours after perforation they 
numbered 7700. I have been unable to find definite records 
wherein the leukocytes were counted just preceding intestinal 
perforation and at regular intervals after its occurrence. In the 
cases I have studied and in a number reviewed in the Hterature a 
gradvial progressive increase in the number of leukocytes often 
followed perforation ; but a fact to be borne in mind is that perfora- 
tion may have taken place some hours before the initial counts 
were made, and for this reason particularly I hesitate to accept 
without question the view that leukocytosis is found during the 
first six hours following intestinal perforation. 

The leukocytes are influenced by treatment, as hypodermo- 
clysis, cold baths, drugs, etc. (page loi). The eosinophils are 
decreased or absent during the febrile period, and degeneration of 
the leukocytes, leukocytic shadows, and leukocytes showing 
granules of glycogen are to be seen. 

During the febrile period a progressive diminution in both 
the number and percentage of the polynuclear cells occurs, with 
a corresponding increase in the lymphocytes and large mono- 
nuclear elements. Eosinophils are diminished or absent, but 
increase as convalescence is estabhshed. The percentage of 
polymorphonuclear cells may remain stationary where comphca- 
tions and leukocytosis are present. Generally speaking, the specific 
gravity, hemoglobin, and red cells show the changes common to 
secondary anemia. Among the favorable signs Nagaeli places 
a decided decrease in all forms of leukocytes and the absence 

*" Trans. Phila. Co. Med. Soc," Feb., 1901. 



ACUTE INFECTIOUS DISEASES. 1 35 

of leukocytosis during the existence of complications. Bac- 
teremia may develop. No clinical importance is attached 
to the recovery of typhoid bacilH from the rose spots, since they 
may be cultivated from the skin and perspiration. 

Diphtheria. — The red cells remain normal or above normal, 
except during convalescence, when they show moderate reduc- 
tion. A sHght reduction follows the administration of antitoxin. 
The hemoglobin is but sHghtly reduced — 5 to 10 per cent. 
BiUings* found the diminution less marked in cases treated with 
antitoxin. Anemia and bacteremia may, however, develop (see 
Bacteriology oj the Blood). 

Leukocytosis. — Leukocytosis is an early feature in diphtheria 
and is, as a rule, in proportion to the severity of the disease, 
15,000 to 30,000 per cubic millimeter. It may reach its height 
the second day (severe type) or not until the sixth day, while 
malignant cases often show progressive leukocytosis or leukocy- 
tosis may be wanting. Other throat disorders with equally 
marked symptoms show, as a rule, a higher leukocyte count than 
does diphtheria. The polynuclear neutrophil cells are increased 
and a relative or, at times, actual lymphocytosis may be found. 
Eosinophils are decreased or normal. Myelocytes are present, 
and should they exceed 3 per cent., are of grave prognostic moment. 
"Leukocytic shadows" are common findings, and Ewing demon- 
strated an increased acidophile tendency of the neutrophil granules. 

Scarlet Fever. — The red cells are moderately reduced (3,000,- 
000 to 4,000,000 per cubic millimeter) during convalescence, and 
hemoglobinemia has been observed. There is some distortion 
of the red cells, and normoblasts are occasionally seen. Bac- 
teremia may ensue (see Bacteriology of the Blood). 

White Cells. — Leukocytosis is to be observed early (15,000 
to 30,000 per cubic milHmeter), and even before the appearance 
of the eruption, faUing with the decline of temperature ; but rarely 
it persists for days or weeks after the temperature is normal. 
Over 40,000 leukocytes is of bad prognostic omen. The poly- 
morphonuclear cells are increased (80 to 90 per cent.), early 
returning to the normal in favorable cases. 

Characteristic Feature. — Eosinophiha is present (5 per cent.) 
in all except malignant cases, and persists during convalescence 
until the sixth week, when it may reach from 10 to 20 per cent. 
Eosinophilia is of serious prognostic value in scarlatinal nephritis 
(Neusser), and when absent in scarlet fever myelocytes are to 
be found. 

* "Johns Hopkins Hosp. Bui.," 1894, p. 105. 



136 



THE BLOOD, 



Measles. — The fibrin is increased ^vhen decided inflammation 
of the mucous surfaces is present. The red cells are practically 
normal; and leukopenia may be encountered during the eruptive 
stage. Both the lymphocytes and large mononuclear cells are 
increased during convalescence. The eosinophils are normal or 
diminished during the febrile stage. Cabot found 6000 and 8000 
leukocytes per cubic millimeter in two cases of German measles. 
Weber* recovered a protozoon from the blood of measles. 



DISTIXGUISHIXG HEMATOLOGIC FEATURES OF 
SCARLET FEVER, .-VXD MEASLES 



DIPHTHERIA, 



Diphtheria. 

Leukocytes, 25,000 to 
30,000 and in severe 
and fatal cases these 
cells may number 
50,000 per cubic 
millimeter. 

A relative hTnphocy- 
tosis common; the 
polynuclear cells 
are moderately in- 
creased. 

Eosinophils of normal 
ratio, decreased, or 
absent. 



4. MyelocN-tes present, i 

to 4 per cent. 

5. Leukocytic shadows 

common. 



ScAiLLET Fever. 
I. Leukoc\-tes, 15,000 to 
30,000 or 40,000 at 
the onset and before 
the appearance of 
the eruption. 

2. Polynuclear cells 85 

to 95 per cent.; 
hTuphocytes normal 
or subnormal. 

3. Eosinophils increased 

after second or third 
day; 10 to 15 per 
cent, by the second 
week; return to nor- 
mal the sixth week. 

4. Myelocytes unusual 

findings. 
;. Rare. 



Measles. 
Leukoc}-tes absent; 
leukopenia the rule. 



2. Lymphocytes and 

large mononuclears 
are increased during 
convalescence. 

3. Eosinophils dimin- 

ished the rule. 



4. Absent. 

^. Rare or absent. 



Small-pox. — During the febrile stage of small-pox poly- 
cythemia may prevail, and later, during convalescence, a mild 
grade of chlorotic anemia develop. According to Pick's pains- 
taking research cases of small-pox with moderate eruption showed 
the leukocytes to be normal or subnormal in number. Leukocy- 
tosis develops as a result of suppuration, and may oscillate be- 
tween i2,cxx) and 20,000 or more per cubic miUimeter, increasing 
relatively with the advancing suppuration. In one instance I 
found 30,000 leukocytes per cubic milHmeter six weeks after 
convalescence had been estabhshed. Pneumonia as a com- 
phcation is coupled with a reduction in the number of leuko- 
cytes. Ameboid bodies have been detected in the blood-cells of 
small-pox, measles, and scarlet fever, and have been regarded by 
Weber and Doehle and by a number of other observ'ers as devel- 
opmental stages of a protozoon. See Exudates, pp. 492 and 499. 

*Centralbl. f. Bakt." vol. xxi, No. 6. 



ACUTE INFECTIOUS DISEASES. 1 37 

Vaccinia. — Sobotka (quoted by Ewing) found the red cells and 
hemoglobin to be normal after vaccination. Leukocytosis develops 
on the third or fourth day following inoculation; after which a 
daily fall to the seventh or eighth day ensues, resulting in leuko- 
penia (height of fever). From the tenth to the twelfth day sec- 
ondary leukocytosis develops. In Sobotka's observations the 
primar}' leukocytosis ranged between 12,000 and 23,000 cells 
per cubic millimeter, and the secondary leukocytosis from 10,000 
to 17,500. 

Suppuration {Septicemia, Pyemia, Purulent Cystitis, Osteo- 
myelitis, Abscesses, etc.). — In conjunction with suppurative 
processes wherein the products of suppuration are not firmly 
encapsulated within the human organism leukocytosis develops 
in direct correlation with the degree of infection; such increase 
affecting, for the most part, the polymorphonuclear cells. Leuko- 
cytosis, therefore, together with other chnical findings may be 
invaluable; but its absence does not exclude the existence of 
suppuration. Acute inflammatory processes also induce leuko- 
cytosis; while suppuration of mucous surfaces may excite but 
slight leukocytosis. 

Both the hemoglobin and the red cells are reduced in keep- 
ing with the degree of suppuration; but the hemoglobin is more 
sensitive than the red cells and its loss greater (color-index low). 
The erythrocytes present the changes common to secondary 
anemia. 

Absence of Leukocytosis. — Asthenic cases of septicemia may 
not show leukocytosis and, in fact, may display leukopenia. 

Chemistry. — The hemoglobin at times appears to enter into 
solution with the plasma (hemoglobinemia) when there has been 
great blood destruction. There may also be a tendency toward 
crystalhzation of the hemoglobin, which is detected in the fresh 
blood by crystals forming about the margin of the cover-glass. 
The specific gravity is commonly reduced, and the albumins are 
lowered in proportion to the severity of the infection. Glycogen 
is a rare finding. (For bacteriologic findings see page 113.) 

Appendicitis. — In this disease there appear to be no hemato- 
logic findings that are of great chnical value. A purely catarrhal 
appendicitis is probably seldom placarded by leukocytosis; 
while the majority of severe cases show leukocytosis ranging 
from 12,000 to 25,000 cells per cubic millimeter between the second 
and fourth days. Leukocytosis may be wanting in instances where 
suppuration exists, or vice versa. Judging from the hterature 
(including researches of Cabot and of Deaver and Da Costa) and 
from my own observations upon a rather large series of cases, the 



138 THE BLOOD. 

hematologic findings furnish but Uttle aid in the diagnosis of 
appendicitis. 

Erysipelas. — During the course of erysipelas leukocytosis 
is an almost constant symptom, and in many instances is directly 
proportionate with the type and extension of the infection. In 
fifteen cases examined at the Philadelphia Hospital the leuko- 
cytes numbered from 10,000 to 23,000 per cubic milhmeter upon 
the patient's admission. The polynuclear cells are apt to be 
influenced mostly, and the eosinophils are Hkely to be diminished 
or absent. Bacteriologic study of the blood has proved of no 
chnical value. 

Acute Rheumatism. — In this disease the red cells are Hable to 
moderate reduction while the hemoglobin suffers a greater loss, fall- 
ing to 55 to 75 per cent., and during convalescence the return 
of the red cells to the normal precedes that of the hemoglobin. 

Leukocytosis. — A leukocyte count of from 10,000 to 15,000 
cells per cubic milhmeter represents an average case, but there 
are recorded instances wherein high-grade leukocytosis existed 
in connection with such complications as pericarditis, endocarditis, 
and pneumonia. The proportional relation of the various leuko- 
cytes is rather well maintained in uncomplicated cases; the eosino- 
phils, however, are absent at the onset, present during the dis- 
ease, and increased in convalescence. 

Whooping-cough. — Whooping-cough serves as the only ex- 
ample of an afebrile disease affecting the respiratory tract wherein 
decided leukocytosis is a constant symptom. The degree of leuko- 
cytosis is influenced by the age of the child, and is found to range 
from 20,000 to 40,000 cells per cubic millimeter in uncomplicated 
cases during the active stage; the lymphocytes may range be- 
tween 35 and 55 per cent.; the polynuclear cells are relatively 
decreased; and eosinophils normal or diminished. The hemo- 
globin and red cells bear no direct relation to the degree of leuko- 
cytosis. 

Tonsillitis and Serous Effusions. — Tonsilhtis shows a 
leukocytosis of from 10,000 to 20,000 per cubic millimeter, as 
do also effusions into the serous membranes during the febrile 
stage; and such effusions when they have become purulent show 
a comparative increase in the number of leukocytes. Purulent 
peritonitis may exist without leukocytosis, and when the exudate 
ceases to be poured out, leukocytosis is liable to disappear. Effu- 
sions excited by the tubercle bacillus are infrequently accompanied 
by leukocytosis. 

Influenza. — The most pecuhar feature of this disease is 
that it is of bacterial origin, ushered in with a chill, and does not 



ACUTE INFECTIOUS DISEASES. 1 39 

show leukocytosis. On the contrary, uncompKcated cases are 
Hable to display leukopenia; but when compHcations arise, 
leukocytosis may be encountered. There are no constant changes 
to be observed in either the red cells or the hemoglobin. I was 
unable to recover Pfeiffer's bacillus from the venous blood examined 
at various stages of the disease (see Bacteriology of the Blood and 
Senim-dia gnosis^ pages 113, 116). 

Bubonic Plague. — It is conceded by all observers that leuko- 
cytosis is present both during the active stage of this disease and 
throughout convalescence, varying from 20,000 to 50,000 or more. 
Of these, the polynuclear cells are mostly concerned, and next 
in order are the lymphocytes. The eosinophils are normal or 
decreased (see Serum-diagnosis and Bacteriology of the Blood, 
pages 114, 124J. 

Malta Fever. — In addition to the agglutinative properties 
of the serum in this disease (see Serum-diagnosis, page 125) 
Musser and Sailer* have found the red cells to be normal in 
number, the leukocytes sHghtly increased, and the hemoglobin 
reduced to 60 per cent. 

Yellow Fever. — In this condition the globuKcidal properties 
of the serum are increased, the red cells approximately normal, 
while the hemoglobin suffers severe destruction, faUing to from 
75 to 50 per cent. Leukocytosis may be present; eosinophihc 
cells are normal or reduced ; and myelocytes rarely found. Ewing 
refers to two cases showing hemoglobinemia. 

Gonorrhea. — Uncomplicated cases of gonorrheal urethritis 
exert shght influence, if any, upon the red cells or the hemoglobin, 
but in the presence of complications these may be affected. Leu- 
kocytosis is likewise produced by compHcations and may obtain 
in uncompKcated cases. Extension of the inflammatory process 
to the deep urethra, epididymis, etc., may induce a high per- 
centage of eosinophils. Occasionally the gonococcus invades 
the circulation (see Bacteriology of the Blood, page 114). 

Actinomycosis. — The pulmonary form of this disease may 
show 20,000 or more leukocytes per cubic millimeter, as exempli- 
fied by Ewing's case.f A chlorotic form of anemia has been 
observed by Bierfreund. 

Anthrax and Glanders. — Bacteremia rarely develops during 
the course of anthrax (see Bacteriology of the Blood, page m), and I 
have been unable to discover from the literature any data as to 
the condition of the red cells, hemoglobin, and leukocytes in this 

*"Phila. Med. Jour.," 1898 p. 1408. 
t"Clin. Path, of the Blood," first ed., p. 291. 



I40 THE BLOOD. 

disease. Cabot has found leukocytosis — ii,6oo to 13,600 — in a 
case of glanders. 

Leprosy. — During the various stages of leprosy polycythemia 
may be found, and is usually ascribable to local stasis (cyanosis). 
Winiarski, in the study of 17 cases, found the red cells above 6,000,- 
000 per cubic millimeter. He also found 2,300,000 and 1,900,000 
cells in two well- advanced cases. The hemoglobin ranged be- 
tween 80 and 118 per cent, in all but the two cases showing a 
low number of red cells. The leukocytes were normal or sub- 
normal in number, and the lymphocytes increased, maximum 
of 47 per cent.; but lymphocytosis did not exist in connection 
with suppuration. Brown obtained similar results in 16 cases. 

In a case studied at the Medico- Chirurgical Hospital, through 
the courtesy of Dr. J. V. Shoemaker, I found the hemoglobin 
65 per cent., red cells 3,460,000, white cells 6800, per cubic milli- 
meter. The erythrocytes were deficient in color, staining feebly 
as a rule, though many of the smaller cells stained deeply. De- 
cided variabihty in size and form of the red cells existed, among 
which macrocytes were predominant. 

Nucleated Red Cells. — While counting 200 leukocytes, 40 
nucleated red cells were found, and of these 30 were normoblasts 
and 10 megaloblasts; many of the latter variety showed well- 
marked polychromatophihc properties. A differential leukocyte 
count gave polymorphonuclears 60.2, transitionals 13.9, eosino- 
phils 8.7, small lymphocytes 4.3, large lymphocytes 9.5, large 
mononuclears 3.4 per cent. Leukocytosis was not present in the 
cases examined by Brown or those examined by Winiarski. 

Bacilli. — Lepra bacilli were detected in the circulating blood 
in my case* (see Bacteriology of the Blood, page 112). 

Takosis. — A contagious disease of goats which is excited by 
a diplococcus (Micrococcus caprinus) which invades the tissues 
and is found in the blood during the various stages of the disease. 
J. R. Mohler and H. J. Washburn f describe the blood findings 
in this condition. Smears made from the peripheral blood may 
show the diplococcus, which is always detected in the plasma 
and never situated within the blood-cells. Cultures obtained 
from the peripheral and venous circulations antemortem and from 
the heart's blood and the viscera at postmortem will be found to 
develop the Micrococcus caprinus. Persons who skin animals 
dead of takosis become infected and develop initial blebs and ab- 
scesses. The Micrococcus caprinus is found in the exudates from 
these lesions. 

*"Proc. Phila. Co. Med. Soc," Jan., 1903. 

t" Bureau of Animal Industry Bui.," 1903, No. 45. 



ACUTE INFECTIOUS DISEASES. I4I 

The number of erythrocytes are increased from one to two 
millions per cubic miUimeter (9,000,000 to 10,000,000 normal for 
the sheep) ; and the leukocytes are increased from 9000 to 10,000 
(normal) to 18,000 to 20,000, which increase affects the polymor- 
phonuclear and eosinophilic cells. 

Hemocytolysis. — In this condition the isotonic tension of 
the plasma may be reduced below that of the red cells, when 
the hemoglobin is liable to be extracted from the erythrocytes 
and dissolved in the plasma, leaving a mere shadow of a once 
deeply colored red cell. Again, without appreciable diminution 
in the isotonic tension of the plasma, the erythrocytes undergo 
disintegration and are broken into fragments. The injection of 
a large quantity of normal salt solution into the circulation may 
excite the former condition, while virulent blood poisons produce 
the latter. The two conditions, however, often go hand-in-hand, 
and are to be seen in diverse degrees in various types of anemia. 
Among the special conditions wherein the blood-cells suffer such 
rapid and extensive destruction should be mentioned high tem- 
perature, poisoning by guaiacol, nitroglycerin, amyl nitrite, nitro- 
benzol, fumes of arseniureted hydrogen, snake venom, and the 
ingestion of toad-stools. All these conditions tend not only 
toward the destruction of the red cells, but likewise to the pro- 
duction of hemoglobinemia (see Hemoglobinemia, page 42) and, 
as a consequence, hemoglobinuria. Potassium chlorate, chromic 
acid, antif ebrin, pyrogalHc acid, and CO, when administered in toxic 
quantities, are capable of effecting essential destructive changes 
in the hemoglobin, and similar changes are also seen following 
severe malarial intoxication. As a rule, when the above changes 
occur in the blood, the red cells are decidedly lessened, but because 
of the fact that the hemoglobin, though extracted from the red cells, 
is retained in the serum, this percentage of hemoglobin may not 
be greatly reduced, yet a decided impoverishment, as a rule, 
soon follows. Cases have been recorded, however, wherein the 
hemoglobin suffered decided reduction. The coagulability of 
the blood may be increased, and the alkalinity moderately lowered. 
The reports of clinical observations available for criticism are 
too scanty to warrant deductions. 

Purpura Hsemorrhagica. — This condition is doubtless not 
infrequently of bacteriologic origin (see Bacteriology oj the Blood, 
page 114), yet many cases are recorded wherein no evidence of bac- 
teremia existed, which separates the disease into two classes. Pur- 
pura developing during the course of an infectious disease shows 
but slight reduction in the red cells; but in more severe cases 
absolute diminution may ensue. Microcytes are numerous. 



142 THE BLOOD. 

nucleated red cells occur, and the color-index is low. Poly- 
chromatophilia, leukocytosis, and eosinophilia are of less common 
occurrence. Ewing noted 56,000 leukocytes per cubic millimeter. 
Coagulation is feeble, and many writers refer to a reduction in 
the blood-plates. Other competent observers, however, have 
not been able to confirm this finding. 

The non-infectious type may hematological^ resemble perni- 
cious anemia, the differential feature being that in purpura 
haemorrhagica there is an absence of megaloblasts; normoblasts 
are scanty, and microcytes numerous. Leukocytosis does not 
occur in this form of purpura; but the lymphocytes occupy from 
75 to 90 per cent, of the total number of leukocytes. The red 
cells fall rapidly to 2,000,000, 1,000,000, or less per cubic milH- 
meter. The majority of the erythrocytes are undersized, oval, and 
in the latter respect resemble those in pernicious anemia. 

Scurvy. — The morphologic changes displayed by the blood of 
scurvy are similar to those observed in ordinary anemia following 
hemorrhage. The red cells fall to 3,000,000 or less, and fragments of 
disintegrated cells are to be seen. The hemoglobin index is reduced. 
Leukocytosis has been observed by a number of investigators, 
while many have been unable to detect leukocytes beyond the 
normal maximum hmit. 

Hemophilia. — In hemophiha decreased coagulation of the 
blood has been observed, and was found to be the only hemato- 
logic change conspicuous in a case studied through the courtesy 
of Dr. Ernest Laplace at the Medico-Chirurgical Hospital. 
After the administration of adrenalin chlorid coagulation was 
found to be more rapid. The fibrin is about normal in amount. 
Further blood changes are usually the result of hemorrhage, 
and to arrive at any definite conclusions the blood of hemophilia 
must needs be studied when the bleeder is apparently in perfect 
health (see Blood- plates, page 100). 

Addison's Disease. — In Addison's disease the red cells are 
commonly diminished to from 2,000,000 to 3,000,000 per cubic 
millimeter. Microcytosis is conspicuous; the leukocytes are nor- 
mal or subnormal, and of these, eosinophils occupy the high nor- 
mal percentage. 

Myxedema. — Myxedema when uncomphcated and not sub- 
jected to treatment displays a secondary chlorotic anemia, with a 
mild grade of leukocytosis. The hemoglobin registers 60 to 70 per 
cent, or less, and the red cells are found to be greatly reduced. The 
administration of thyroid extract may be followed by appreciable 
improvement in the hematologic tissue, which may result even 
in polycythemia. 



PARASITIC DISEASES AFFECTING THE BLOOD. 1 43 

PARASITIC DISEASES AFFECTING THE BLOOD. 

UNCINARIA DUODENALE (ANKYLOSTOMA DUODENALE). 

Infection with this parasite usually results in a profound 
anemia, which is characterized by a low percentage of hemo- 
globin and low color-index; red cells 1,000,000 or less in severe 
cases, and poikilocytosis well marked. Normoblasts are fre- 
quently encountered, and in extreme instances megaloblasts 
are not uncommon findings. In uncomphcated cases the leuko- 
cytes are normal, and eosinophilia commonly pronounced, though 
by no means a constant feature of the blood of uncinariasis. The 
blood changes are set forth by Surgeon Bailey K. Ashford, pages 

144, 145- 

The corpuscles of patients suffering from ankylostomiasis are 
easily agglutinable. The serum of persons thus infected is more 
actively hemolytic for the blood of rabbits than is normal blood; 
but is not hemolytic for either healthy or pathologic bloods of 
man. Serum from persons infected with the uncinaria is highly 
toxic for rabbits, inducing hemoglobinuria and often causing 
death (Romanis).* 

STRONGYLOIDES INTESTINALIS. 

Strongyloides intestinalis is not infrequently associated with 
the ankylostoma. Ewing cites Teissier as having reported the 
discovery of numerous embryos of the anguillula in the blood of 
intermittent fever. Moderate eosinophilia — 10 to 13 per cent. — 
has been observed. (See p. 419.) 

ASCARIS LUMBRICOIDES, OXYURIS VERMICULARIS, 
TRICHOCEPHALUS DISPAR. 

These parasites are capable of producing a severe grade of 
secondary anemia. The trichocephalus is associated with ankylos- 
tomiasis, and its ova have been present in the feces in all cases 
of ankylostomiasis studied by the author. Fatal anemia may 
follow infection with any of these parasites, when the red cells 
may number below 2,000,000 and the hemoglobin 40 per cent, 
or less. -Leukocytosis is seldom observed, but eosinophiha is a 
common finding in cases of Ascaris lumbricoides. I have re- 
peatedly found the eosinophils between 10 and 18 per cent, in 
children infected with the oxyuris, but it was impossible to say 
definitely that this eosinophilia resulted from this parasite alone, 
since these children were always of lowered vitality, anemic, and, 
being hospital cases, blood examinations after the institution of 
treatment were not feasible. 

* " Gazzetta Degli Ospedali e Delle Cliniche," Nov. 27, 1904. 



144 



THE BLOOD. 



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PARASITIC DISEASES AFFECTING THE BLOOD. 



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146 



THE BLOOD. 



TRICHINOSIS. 

Infection with the Trichina spiraHs usually causes eosinophilia 
(15 to 50 per cent.) to develop with the onset of the symptoms, 
and to continue for weeks and months after the acute manifesta- 
tions have subsided. There appear to be but few records wherein 
the blood of trichinosis has been studied for eosinophiha after 




Fig. 48.— I, Bovine blood fluke (Schistosoma bovis),male and female (after Leuckart); 
2, ova of bovine fluke (after Sonsino); 3, human blood fluke (Schistosoma haematobium), male 
and female ; magnified (after Looss). 



the patient had supposedly recovered. In one case observed the 
eosinophils were at a high normal hmit one year after the onset 
of the disease. Increase of the eosinophils is accompanied by 
a reduction in the neutrophil cells, and vice versa. 

Leukocytosis is not an uncommon symptom, yet by no means 
is it a constant one. Brown found the leukocytes to number 



FILARIASIS. 147 

35,700 in one instance. In my own case they never numbered 
above 7500. The hemoglobin may fall from 75 to 50 per cent., 
and the red cells at the onset number 4,000,000 or more; but 
when the infection is severe, the erythrocytes are markedly reduced 
from the sixth to the tenth week of the disease. Trichinosis 
cannot be diagnosed upon the blood findings alone, and all im- 
portance is attached to the detection of the embryos in the muscle 
tissues (see Trichinosis, page 422). 



SCHISTOSOMA (DISTOMA, BILHARZIA) H^MATOBIUM. 

The adult parasites (Fig. 48, 3) inhabit the veins of the portal 
system, where they are to be found in great numbers. Their 
ova seldom enter the general circulation, however, but are to be 
found in the veins of the rectum and of the bladder. Ulceration 
of the mucous surfaces ensues when the ova (Fig. 48 and Plate 
19 A) escape and are found entangled in the blood-clots of the 
urine or of the feces (see Parasitic Hematuria, page 295). Anemia 
may follow hemorrhage from the bladder, which is apt to be 
persistent, continuing for a period of several years. Early after 
infection eosinophiHa has been detected. 



DIBOTHRIOCEPHALUS LATUS, T^NIA SOLIUM. AND T^NIA 
MEDIOCANELLATA. 

A severe secondary anemia may result from infection with 
any one of these parasites. The bothriocephalus is claimed 
by foreign authors to excite an anemia resembhng closely, if 
not identical with, pernicious anemia. In the study of a number 
of persons infected with the beef tape- worm I have always found 
a rather high-grade secondary anemia. In three of these cases 
normoblasts were found. 

FILARIASIS. 

The Filaria sanguinis hominis (Fig. 49) is a nematode worm 
which inhabits the deeper blood-vessels or lymphatics, and usually 
discharges its embryos into the circulating blood, yet by no means 
are embryos found in the blood in all cases of filarial infection. 
According to Manson's classification, the embryos are most numer- 
ous in the blood at certain periods, and he has named the different 
organisms, with reference to their periodicity: Filaria diurna, 
which occupies the deeper vessels during the night and invades 
the circulation during the day; Filaria nocturna, which courses 
through the peripheral circulation at night; and the Filaria per- 



148 



THE BLOOD. 



stans and Demarquaii, which are present in the circulation both 
by day and by night. 

Method of Detection and Staining.— Special Technic for 
the Study of the Filaria (see page 74). — In smearing blood 
upon sHdes or cover-glasses it is well that films be made rather 
dense in order to include several organisms upon a single shde. 
Fix the blood by heat, stain one-half minute with a 2 per cent, 
solution of eosin in 70 per cent, alcohol, and counterstain with 
a 2 per cent, solution of methylene-blue for from one-half to two 
minutes — the operculum will display a hght-pink tinge, while 
the inclosed parasite stains blue. The filaria is readily detected 




Fig. 



49. — Filaria sanguinis hominis. Living filaria in blood from case at Pennsylvania 
Hospital. Sketch forty-eight hours after blood was taken. 



in the stained specimen even by the inexperienced eye, and to 
those not famiHar with the parasite this method of research is 
commendable In searching for the Hving embryos in the fresh 
specimen of blood a two-thirds objective should be employed, 
under which they appear as minute wrigghng serpents. After 
the parasite is located with a low-power objective it may be 
studied in detail through a one-sixth or a one-eighth objective. 

Clinical Significance. — The filaria is an etiologic factor in 
parasitic elephantiasis and in chyluria. The Filaria perstans 
has been found repeatedly in the blood of persons suffering from 
sleeping sickness, but no alhance has been proved to exist between 
filariasis and sleeping sickness (spinal trypanosomiasis, page 151). 



DRACUNCULUS MEDINENSIS. 



149 



DRACUNCULUS MEDINENSIS (GUINEA-WORM)* 

Dracontiasis, or guinea- worm disease, like filariasis, is a tropic 
affection caused by the Dracunculus medinensis ; the aduk parasite 
inhabiting the human connective tissue, and belonging to the class 
of nematodes (Fig. 50, B). Its habitat is the western coast of 




Fig- 50- — ^, Embryo of guinea-worm (Dracunculus medinensis); B, adult female guinea- 
worm (after Bristow). 



Africa, India, Brazil, and Arabia. According to statistics, a single 
authentic American case has been reported by Edward Francis,* 
though there appear records of two additional cases. The adult 
female worm is cylindric, about 26 inches in length, and one- tenth 
of an inch in diameter, of a milky color, smooth surfaces, with 

* " Amer. Med.," Oct. 26, 1901, p. 651. 



I50 



THE BLOOD. 



a tapering tail that is abruptly bent near its tip. The head is 
provided with a triangular mouth surrounded by six papillae. 
The uterus extends nearly from the head to the tail, and is filled 
with embryos. R. H. Charles discovered a worm in the mesen- 
tery of a cadaver, and regarded it as the male of the Dracunculus 
medinensis. The exact method of infection with this parasite re- 
mains moot, though the cyclops, a small crustacean, probably 
serves as an intermediate host. 
The Embryo. — The embryo 



is 



nearly one-half of an inch 
in length, — 5 to 75 mm. 
by 0.015 ^o 0.025 mm. 
(Manson) (Figs. 50, 51), 
— its head tapers shghtly, 
and the tail is long and 
sharply pointed. The ali- 
mentary canal is readily 
distinguishable. The im- 
pregnated female makes 
her way through the intra- 
cellular connective tissue 
for the period of from 
nine to twelve months, 
and when fully matured, 
she burrows her way to- 
ward the legs and prob- 
ably to the feet, and now 
appears near the surface 
of the body and emerges 
from the derma. The 
uterus ruptures and the 
embryos are discharged in 
a whitish fluid. Symp- 
toms of the guinea-worm 
do not develop until the 
parasite is fully matured, when the initial feature is the appear- 
ance of a vesicle or abscess at the site where it emerges through 
the skin. This may be preceded for a few days by localized swell- 
ing, a feehng of tension, sensitiveness, and redness, and in many 
instances the worm may be felt beneath the skin. Developing 
from the abscess is an ulcer which is more or less extensive, and 
from which the head of the adult parasite may protrude. 

Detection. — The milky discharge collected from the ulcer, 
when placed upon a sHde and studied microscopically, will be 
found to contain a number of embryos (Fig. 51); and when 




Fig. 51. — Embryo Dracunculus medinensis (guinea- 
worm), highly magnified (after Francis). 



TRYPANOSOMIASIS. 151 

spread upon a slide, fixed by heat, and stained with carbol-thionin, 
they may be mounted in Canada balsam. Should the embryo 
be mounted in Canada balsam without staining it will be impos- 
sible to detect the parasite (Francis). 

TRYPANOSOMIASIS. 

(Surra; Tsetse-fly Disease; Nagana; Mai de Caderas; Doorine; Mai de Coit; 

Pjudi.) 

The trypanosoma is a flagellated hematozoon which has been 
found in the blood of man along the Gambia River, in Algiers, 
and a case, the fourth, in which the parasite was detected is re- 
ported by Dr. Le Moal as having occurred in the French Congo.* 
It is not unlikely that the commissions authorized by the 
various European governments for the investigation of malaria 
in South African colonies and tropic districts will furnish valu- 
able data regarding the frequency of the trypanosoma in man. 
Mansonf has outlined the clinical pictures of two cases of trypano- 
somiasis, and in view of his descriptions it seems fair to believe 
that the disease is more common than would appear on first con- 
sideration. The parasite is to be found in the blood from the 
peripheral circulation during the febrile stage of the disease, but 
during the afebrile period it is seldom encountered, though they 
become numerous at each successive recurring pyrexia. From 
one to six parasites may be counted in a three-fourths of an inch 
blood-film prepared during the febrile stage. Thus far no re- 
lation has been found to exist between the degree of temperature 
and the number of parasites present in the blood. 

The Parasite. — In size, the Trypanosoma hominis varies from 
18 to 26 /i in length, and from 2 to 2.5 /^ in breadth. In the pe- 
ripheral blood are to be seen large, roundish bodies 14 to 16 fi in 
diameter, showing one or more vacuoles which are usually regarded 
as being a developmental stage of the parasite (Fig. 52). The 
structure and habit of the Trypanosoma hominis resemble the 
trypanosomes common to the blood of the lower animals, among 
which may be given rats, rabbits, cats, dogs, mice, bats, monkeys, 
horses,- mules, cattle, camels, elephants, buffaloes, and sheep. 
Trypanosoma gambiense (Button) is a minute, colorless, trans- 
lucent, active vermicule, tapering toward its extremities, the an- 
terior of which is provided with a long flagellum — a continuation 
of an undulating membrane attached for nearly the entire length 
of one side of the body — which is of alveolar structure (Figs. 

* "Le Caducee," Dec. 20, 1902. f "Tropical Diseases," third ed., p. 178. 



152 



THE BLOOD. 



52, 53). That portion of the parasite which may be regarded 
as the body often shows indistinct minute granules and "very 
generally a refringent speck, a centrosome, near the posterior 
end." The trypanosoma is found free in the plasma and has not 
been seen within the corpuscle. E. J. Moore,* while making 
daily examinations of the blood of infected persons — natives of 
West Africa — believes that certain peg-shaped bodies seen in the 
red cells represent the intracorpuscular parasite. These comma- 
shaped refractile bodies are also seen in the plasma. Manson 
has observed parasites displaying evidence of longitudinal division. 
For demonstration of this parasite in laboratory work the blood 
of rats will be found to serve adequately this purpose, since they 




Fig. 52. — Trypanosoma from blood of gray rat; also nodular cells, probably preparing for 

division. 

are usually infected with a form of trypanosoma. Inoculation of 
susceptible animals with the blood of infected rats is capable of 
producing the disease. 

The technic for the recognition of the Trypanosoma hominis 
differs in no way from that given for the detection of the malarial 
parasite in the fresh blood (page 157). It is seen best with an 
oil-immersion objective, and is indistinguishable unless magnified 
300 diameters or more. F. G. Novoy has cultivated the trypan- 
osoma of rats on a medium composed of rabbit's blood-serum 
and agar. Growth occurs in the condensation hquid, but not 
upon the surface of the medium. f 

*" Lancet," Oct. i, 1904. 

t " Jour. Amer. Med. Ass.," June, 1902, p. 1653. 




MALARIA. 153 

Staining. — The Trypanosoma hominis is stained by the ordi- 
nary aniHn dyes. I prefer the following method: Smear the 
blood rather thinly and fix by heat, when stain for from one- 
half to one minute with solution of i per cent, eosin in 70 per 
cent, alcohol, wash in water, and stain for fifteen seconds with a 
2 per cent, aqueous solution of methylene-blue, wash in water, 
and again stain for five seconds with eosin, wash, and mount 

Sleeping Sickness.— Aldo Castellani detected the trypanosoma 
in the cerebrospinal 
fluid obtained by lum- 
bar puncture from a 
case of sleeping sick- 
ness in 1892, and has 
since found this para- 
site in the cerebro- 
spinal fluid of 34 addi- 
tional cases,* and in 

the blood in one in- x'X. 

stance (see Ftlana " * ^^ ^ ^ 
Persians J page 148). 

Bruce obtained 
spinal fluid by lumbar V - ,;^23b»-V 

puncture from 38 cases 
of sleeping sickness _. _ . ., . . . . 

■, ■, J Fig- 53- — Trypanosoma from blood of gray rat ; stained 

and detected the try- with a 2 per cent, aqueous solution of methylene-blue. 

panosoma in the fluid 

from every case. The parasite was also found in the blood of 
12 out of 30 cases thus studied. Chatterjeef found a trypan- 
osome in the proboscis of a mosquito. 

Animals. — Musgrave and Wilhams estimate the loss by death 
of horses in the Phihppine Islands from "surra" (trypanosoma 
infection) at $2,000,000 a year. J The symptomatology of animals 
has suggested to me that possibly certain cases of the so-called 
"non-parasitic elephantiasis" were in reality trypanosomiasis. 

MALARIA. 

ZOOLOGIG AFFINITIES. 

Entering upon a study of the malarial micro-organism (hema- 
tozoon of Laveran) it appears warrantable first to direct the 
student's attention to the zoologic affinities of this animal para- 
site, and to the resemblances known to exist between this and other 
allied blood parasites. 

*" Lancet," June 20, 1903. t " Indian Medical Gazette " Oct., iQor. 

t Dept. of the Interior, U. S. A., 1903. 



154 THE BLOOD. 

Zoologically, the hematozoon of Laveran belongs to the class 
of sporozoa and is somewhat closely allied to the coccidia (Plate 24, 
page 388). On account of certain pecuharities common to the 
malarial parasite and to other parasites of the lower animals it 
has been classed with these parasites in the special orders, which 
have been appropriately named hemameba, hemamebida, hemo- 
sporidia, etc. The malarial parasite resembles the coccidia in 
that a portion of its life is spent within the body-cell of the host, 
selecting especially the red blood-corpuscle for this portion of its 
life-cycle. 

Up to the present time the malarial parasite is not known to 
affect other vertebrates than man; but parasites closely allied 
to the malarial micro-organism invade the blood-corpuscles of 
vertebrates — viz., dog, bat, monkey, horse, birds, and cattle. 
Little is known regarding these parasites except of the Pirosoma 
bigeminum (Fig. 55), the cause of Texas fever in cattle, which 
has been extensively studied by Theobold Smith, of America. 

The animal parasites invading the blood plasma and the 
corpuscles of birds and reptiles, such as halteridium, proteosoma, 
and drepanidium, have of recent years received careful study. 
The vast amount of light thrown upon the true life-cycle of the 
malarial parasite through the comparative study of the parasites 
of other vertebrates is evidenced by the fact that MacCallum 
discovered the method of sexual fertilization of the malarial 
organisms while studying the blood of birds infected with the 
halteridium (Fig. 54). According to Laveran, these animal para- 
sites (haemocytozoa) were arranged under three subclasses. 

I. HEMAMEBA. — A genus characterized by the development of 
pigment and by an asexual (endogenous) and a sexual (exogenous) 
life-cycle (Fig. 66). The sexual or exogenous cycle is completed 
through the agency of the mosquito. This genus includes the 
malarial parasite. 



Names. Hosts. 

H. subtertiana ] TThe malarial parasites of man, the sexual 

H. tertiana >■ < phase being evolved in mosquitos of the 

H. quartana j [ genus anopheles. 

H. (Proteosoma) relicta. Birds; sexual phase in mosquitos of the genus 

culex. 
H. (Halteridium) Danilewskyi ..Birds; sexual phase probably the mosquito. 
H. Kochi Several species of monkey; sexual phase not 

determined. 
H. melaniphera Bat (Miniopterus Schreibersii) ; sexual phase 

not determined. 
H. Metchnikovi Trionyx indicus; sexual phase not determined. 

2. PiROPLASMA. — The specics of this genus are devoid of 
pigment and have an asexual (endogenous) reproduction, prob- 
ably effected by binary division, and a sexual phase of develop- 



PLATE 10. 






D 




PiROPLASMA HOMINIS. 

I, Small form of the parasite found in one field; 2, the same, another field; 
3, showing parasite with central stained spot surrounded by a vacuole. (Figs. 
1-3 stained with Wright's stain, followed by LofSer's blue. X 750.) 

4, 5, Small form of the parasite (X 665); 6, large form (X 665); 7 and 8, 
single form of the parasite (X 1000); 9, double form of the parasite (X 1000); 10, 
one field showing two infested corpuscles ( X 665); 11, one field showing a corpuscle 
with a large and small parasite ( X 1000) (Figs. 4-1 1 from fresh blood) (Anderson). 



MALARIA. 155 

ment which takes place in various species of tick. In human 
piroplasmosis the parasites are found in the peripheral blood, 
in that from the viscera, bone marrow, and the exudate from 
skin and intestinal ulcers. In the red cells they are usually 
situated near the periphery. They are oval, bacillary, or pear- 
shaped, and measure about one fj. in diameter. Organisms are 
not numerous in the capillary circulation (Plate 10). 

Names. Hosts. 

P. bigeminuin Bovines; transmitted by the cattle-tick (Boophilusbovis). 

P. canis _Dogs. 

P. ovis Sheep. 

P. equi Horse. 

P. hominis -Man. 

-D 1 • • r ^ • ) Transmitted by the tick (Dermacentor reticulatus). — 

P. hominis of mountain ^t^- ^ju * u c r^i 

^^ ^ r y JNot contirmed by more recent researches of Chas. 

spotted fever f ^v^.^ell Stiles. 

3. H^MOGREGARiNA. — The specics of this genus infest the 
blood of cold-blooded vertebrates, viz., frogs, hzards, snakes, etc. 
They may assume the form of vermicules, and may be found 
either within the red corpuscle or free, swimming in the plasma 
(Fig. 56). The life-cycle of this genus is unknown. 

Names. Hosts. 

H. (Drepanidium) ranarum ^ 

H. splendens \ Frog (Rana esculenta). 

H. magna J 

H. lacertarum Lizard (Lacerta muralis). 

4. Proteosoma and Halteridium. — These pigmented para- 
sites are known to invade the blood-corpuscles of birds. The 
student should compare figure 54 with plate 1 1 in order to appre- 
ciate fully the resemblance between these micro-organisms and 
that of malaria. Both these bird parasites have an asexual (en- 
dogenous) cycle of development. The proteosoma has its sexual 
development in the mosquito (culex), and the halteridium is 
doubtless transmitted in some allied manner. 

The study of these parasites is readily accomplished by study- 
ing the blood of sparrows; the halteridium is common in the 
blood of doves, pigeons, and crows. Cleanse the inferior surface 
of the bird's toe, make a puncture near the tip, and continue the 
study as for malarial parasites (page 157). 

5. Pirosoma Bigeminum. — This animal parasite is con- 
cerned in the production of Texas cattle fever, a disease most 
destructive to the lives of the bovine family in the southern United 
States, Europe, South Africa, and Australia. The Pirosoma 
bigeminum (Fig. 55) is devoid of pigment and is to be found in 
the red blood-cell. Two parasites may occupy a corpuscle. 
It remained for Theobold Smith to discover that the pirosoma was 



iS6 



THE BLOOD. 



transmitted from one vertebrate host to another by the cattle- 
tick (Boophilus bovis). In feeding upon the blood of infected 




Fig. 54. — Halteridium form of the parasite of birds : i, Adult granular or female form ; 2, 
adult hj'aline or male form; 3, adult female preparing for extrusion from the corpuscle; 
4, adult male preparing for extrusion from corpuscle ; 5, adult female extruded and lying 
beside the nucleus of a corpuscle ; 6, flagellate form ; 7, process of fertilization ; 8, first stage 
in formation of motile form ; 9, fully developed motile form or vermiculus ; 10, fully developed 
motile form in process of disintegration (from original illustrations by W. G. MacCallum, 
"Jour. Exp. Med.," 1898, p. 136). 



cattle the tick takes in the parasite and in some unknown manner 
infects her ova. Young ticks hatched from this infected mother 
tick's eggs infect healthy cattle through their bites, a circumstance 



THE MALARIAL PARASITE. 



157 



somewhat analogous to the transmission of malaria by the bite of 
the mosquito. 

6. Drepanidium. — This is a non-pigmented blood parasite 
of frogs (Fig. 56), which is found both as an endocorpuscular, 



/^?^^ /*^^ ^/^^^.^ 




Fig- 55- — Pirosoma bigeminuni in bovine blood (after Celli). 

non-motile body and also free in the plasma. The free parasite 
may display movement. 

THE MALARIAL PARASITE. 

Method of Examination. — Collect the blood as described 
on page 33 from the tip of the finger or the lobe of the ear. The 
drop should not be too large, and this can be estimated only by 
sufficient practice to enable one to place beneath the cover-glass 



\ 



Fig. 56. — Drepanidium ranarum : i, Parasite within the red cell; 2, 3, extracellular motile 

(forms after Celli). 




just enough blood so that when spread between the cover-glass 
and shde a film of such thickness results as to hold the cells in 
close proximity, not touching, and equally disseminated through- 
out the field. The malarial parasite, a small hematozoon situ- 
ated within the red corpuscle, may be hyahne, granular, or pig- 
mented, and its contour is circular, oval, or irregular. After 
it has destroyed the hemoglobin of the red cell the parasite be- 
comes swollen, pale, and granules of pigment displaying Brown- 
ian movement are seen within its body, which at times occupies 



158 THE BLOOD. 

nearly the entire red cell. The various forms of malarial hemato- 
zoa are best shown by the accompanying illustrations (Plates 

11-13)-. 

Staining of the malarial parasite is not essentially different 
from that of staining ordinary blood smears. The films are 
spread in the same manner, dried in the air, and later may be 
fixed in any of the methods described for fixation of the blood 
(page 74). Futcher recommends immersing the dried films in 
a 0.25 per cent, solution of formalin in 95 per cent, alcohol for 
one minute, after which rinse in water. However the fixing may 
be accomplished, the malarial parasite is well stained by a car- 
bolated solution of thionin, and by this solution it appears as 
a conspicuous, reddish- violet body. 

Carbol-thionin. — Carbol-thionin is prepared as follows: Satu- 
rated solution of thionin in 50 per cent, alcohol, 10 c.c. ; aqueous 
solution of phenol (1-40), ico c.c; when mixed, keep in a colored 
bottle. This stain is of special service in the staining of ring- 
shaped bodies found in estivo-autumnal fever, and which do not 
stain well w^ith eosin and methylene-blue. Jenner's stain is also 
invaluable for the detection of the malarial parasite (see Jenner^s 
Stain, page 78). 

Eosin and Methylene-blue. — Eosin and methylene-blue will 
also be found capable of staining blood and malarial parasites 
in a manner which will render the latter conspicuous. Plehn 
suggested the following stain, which has been rather generally 
employed : 

Concentrated aqueous solution methylene-blue ..60 c.c. 
Solution of eosin in 75 per cent, alcohol (0.5 per 

cent. ) 20 " 

Distilled water 40 " 

Aqueous solution of sodium hydrate (20 per cent.) . 12 drops. 

After mixing, the films are stained for five to six minutes, 
washed in water, dried, and mounted. By Plehn's method the 
red corpuscles are stained pink (eosin), while all nuclei and the 
malarial parasites stain blue. 

Wright's Method. — At the suggestion of Dr. Thayer, of Johns 
Hopkins University, the late Dr. Jesse W. Lazear, in study- 
ing the structure of the malarial parasite when stained according 
to Nocht's method, gives the accompanying illustrations (Plate 
13). Wright's method is but a practical adaptation of the method 
of Nocht; and while there are several apparently wide differences 
in the technic of these methods, they have been found to give 
similar results. 

Reference to Wright's method of staining (page 78) and to 



Description of Plate ioa. 

Zygotes of Bird Malaria and Human Malaria : Figs. 1-3, zygotes of bird malaria 
(proteosoma, Labbe) about two or three days old, developing in middle intestine 
(stomach) of mosquito (Culex). The specimen of infected mosquito was obtained 
by Dr. Ronald Ross in Calcutta, India, July 12, 1898, and through courtesy was 
loaned to Dr. Albert Woldert, who made the dravv'ings. The three figures are from 
the same specim^en and represent different degrees of magnification. Fig. i, middle 
intestine (stomach) of mosquito, showing zygotes lo // in diameter (No. 3 oc. No. 3 
lens) (Leitz). Fig. 2, same as Fig. i, showing ten zygotes of proteosoma about 10 /z 
in .size in one field, yL oil immer. lens, No. 3 oc. (Leitz). Fig. 3, the zygotes Nos. 
1-3 shown in Fig. 2, greatly magnified, and diagrammatic, showing yellowish hyaline 
capsule and yellowish hyaline, oval-shaped masses (fatty granules?) and vacuoles. 
Protoplasm has a reticulated appearance and contains reddish pigment granules. 

Figs. 4-8, zygotes of humrai malaria, four days old, developing in middle intes- 
tine (stomach) of mosquito (Anopheles quadrimaculata or claviger), obtained by Dr. 
Albert Woldert, Nov. 5, 1900 (second successful result in America). Figs. 4-8 are 
from the same specimen and represent different degrees of magnification of zygotes 
derived from estivo- autumnal parasite (case of estivo-autumnal fever occurring at the 
Pennsylvania Hospital, service of the late Dr. F. A. Packard). 



PLATE loA. 






-i<. 









.^ 







/Oa / 








' ^^ 



THE MALARIAL PARASITE. 1 59 

plate 13, with a careful study of its accompanying key, will be 
found to direct even the inexperienced. 

Hyaline Bodies. — Hyaline or non-pigmented intracellular 
bodies represent the earher stages in the development of the mala- 
rial parasite, and are to be found in the blood of all forms of malarial 
infection. They are especially abundant after the paroxysm, 
and often resemble vacuoles, ameboid movements being their 
characteristic feature. This movement is most pronounced in 
tertian fever when the outline of the organism changes with great 
rapidity. This same change is to be detected in the parasites of 
irregular estivo-autumnal fever, but, as. a rule, the estivo-autumnal 
parasite assumes a ring-like appearance, and seldom throws out 
pseudopodia. The number of non-pigmented intracellular hema- 
tozoa is at times very remarkable, and in a case originating in 
Panama and observed at the Philadelphia Hospital every micro- 
scopic field of the fresh blood showed several of these organisms. 

Pigmented Bodies. — The pigmented intracellular organisms 
are doubtless a later stage in the development of the parasite, 
and are likewise encountered in all forms of malarial fever. There 
does not exist, however, that uniformity in the different forms of 
malarial infections that is shown in the hyaline bodies (Plate ii); 
e. g., minute reddish-brown granules often appear in the bodies of 
the tertian organism soon after the paroxysm, and these increase 
in number, while their host, the red corpuscle, becomes progres- 
sively paler until eventually only an indefinite shell or ring of 
the once deeply colored erythrocyte remains. It is not uncommon 
to see aggregations of these granules resembhng bacilh, all pig- 
ment displaying active movement. The parasite continues to 
enlarge in its development during the above steps, and its body 
is now hyahne and may be seen to undergo ameboid changes, 
but these movements are sluggish. The pigment-granules often 
appear to be distributed in small aggregations through the body 
of the red corpuscles, lending the impression that more than one 
organism has invaded the erythrocyte, but through close obser- 
vation these isolated patches of granules are found to be within 
a single organism. Within less than forty-eight hours this malarial 
parasite will be found to occupy the entire red corpuscle, which 
is greatly swollen. The ameboid movements now become less 
and less, though the pigment -granules are often rather active, 
tending to congregate around the periphery of the cell. 

Quartan Fever. — Just following the paroxysm, pigmented 
intracellular bodies appear in the blood of quartan fever, but 
here the individual granules display variation in size, and are 
decidedly darker than are those of the tertian type (Plate ii). 



l6o THE BLOOD. 

In striking contrast to those of tertian fever they are but slightly 
motile, often quiescent, and usually accumulate along the pe- 
riphery of the parasite. Slight ameboid movements are often 
discernible, but these lessen rapidly and cease in from sixty-four 
to seventy-two hours, following which the parasite assumes a 
rounded or oval shape, and occupies but a portion of the red 
cell. Another pecuharity of this form of malarial fever is that 
the erythrocytes are not markedly decolorized, but, on the contrary, 
their normal color may be intensified or they may display a green- 
ish or brassy tinge. The erythrocyte in which the parasite has 
developed is below the normal size, and upon staining, the organ- 
ism is found to be surrounded by a variable (usually narrow) 
zone of cell protoplasm. 

Estivo-autumnal Fever. — Pigmented intracellular bodies are 
likewise found in the blood of estivo-autumnal fever (Plate, 12) 
but differ decidedly from the tertian or quartan parasites previ- 
ously described. Pigment-granules appear after the paroxysm, 
are always scanty, at times only one or two rather dark granules 
are to be detected, and these are usually located near the periphery 
of the cell and displaying but slight, if any, movement. This 
parasite occupies about one-fourth to one-third of the body of 
the red corpuscle, but does not decolorize the cell, which often 
exhibits a brassy tint. 

The corpuscle may be irregular, shrunken, spiculated, or 
crenated. Early during the paroxysm the pigment -granules 
may be congregated at the center of the parasite, and according 
to certain observers, among whom Thayer, of Baltimore, deserves 
mention, this pecuhar arrangement is to be observed in tertian 
and quartan parasites during the stage of segm.entation. 

Segmenting Bodies. — Both the tertian and quartan parasites 
may be studied under the microscope during the process of seg- 
mentation in blood collected just prior to or during the par- 
oxysm. In tertian fever corpuscles will be seen where the hemo- 
globin has been almost entirely destroyed, as is shown by their 
pallor. The parasite becomes more and more granular in ap- 
pearance and the pigment-granules, which at first exhibit move- 
ments, become quiescent and enlarged, displaying a tendency to 
congregate near the center of the organism, where they form in a 
round mass. While the pigment-granules are being deposited 
in the center of the cell segmentation of the surrounding granular 
protoplasm may be observed (Plate 11). 

Beginning at the periphery, dehcate striations are seen to 
extend gradually toward the central pigment mass, these stria- 
tions dividing the protoplasm into a number of rather oval bodies 



DESCRIPTION OF PLATES 11 and 12. 



The drawings were made with the assistance of the camera lucida from specimens of fresh 
blood. A Winckel microscope, objective % (oil immersion), ocular 4, was used. Figures 4, 13, 23, 
24, and 42 of Plate 11 were drawn from fresh blood, without the camera lucida. 

PLATE 11. 

The Parasite of Tertian Fever. 

1.— Normal red corpuscle. 

2, 3, 4.— Young hyaline forms. In 4, a corpuscle contains three distinct parasites. 

5, 21. — Beginning of pigmentation. The parasite was observed to form a true ring hj the con- 
fluence of two pseudopodia. During observation the body burst from the corpuscle, v<^hich became 
decolorized and disappeared from view. The parasite became, almost immediately, deformed and 
motionless, as shown in Fig. 21. 

6, 7, 8.— Partly developed pigmented forms. 
9.— Full-grown body. 

10-14.— Segmenting bodies. 

L5.— Form simulating a segmenting body. The significance of these forms, several of which 
have been observed, was not clear to Drs. Thayer and Hewetson, who had never met with similar 
bodies in stained specimens so as to be able to study the structure of the individual segments. 

16, 17. — Precocious segmentation. 

18, 19, 20.— Large swollen and fragmenting extracellular bodies. 

22.— Flagellate body. 

23, 24.— Vacuolfzation. 

The Parasite of Quartan Fever. 

25.— Normal red corpuscle. 
26.— Young hyaline form. 

27-34.— Gradual development of the intracorpuscular bodies. 

35.— Full-grown body. The substance of the red corpuscle is no more visible in the fresh 
specimen. 

36-39.— Segmenting bodies. 

40.— Large swollen extracellular form. 

41.— Flagellate body. 

42.— Vacuolization. 

PLATE 12. 
The Parasite of ^stivo-autumnal, Fever. 

1, 2.— Small refractive ring-like bodies. 

3-6.— Larger disk-like and ameboid forms. 

7.— Ring-like body with a few pigment-granules in a brassy, shrunken corpuscle. 

8, 9, 10, 12. — Similar pigmented bodies. 

11.— Ameboid body with pigment. 

13.— Body with a central clump of pigment in a corpuscle, showing a retraction of the hemo- 
globin-containing substance about the parasite. 

14-20. — Larger bodies with central pigment clumps or blocks. 

21-24.— Segmenting bodies from the spleen. Figs. 21-23 represent one body where the entire 
process of segmentation was observed. The segments, eighteen in number, were accurately 
counted before separation, as in Fig. 28. The sudden separation of the segments, occurring as 
though some retaining membrane were ruptured, was observed. 

25-33.— Crescents and ovoid bodies. Figs. 30 and 31 represent one body, which was seen to 
extrude slowly, and later to withdraw, two rounded protrusions. 

34, 35.— Round bodies. 

36.—" Gemmation." fragmentation. 

37.— Vacuolization of a crescent. 

38^0.— Flagellation. The figures represent one organism. The blood was taken from the ear 
at 4.15 p. m. ; at 4.17 the body was as represented in Fig. 38. At 4.27 the flagella appeared; at 4.38 
two of the flagella had already broken away from the mother body. 

41-45.— Phagocytosis. Traced with the camera lucida. 

1 These illustrations are reproduced by permission from the article by Drs. Thayer and Hewet- 
son in The Johns Hopkins Hospital Reports, vol. v., 1896. 






The Parasite of Tertian Fever. 



PLATE II, 



-%■ 



V^: ^ 



,.^ 
%*** 



/<9 



.•ft •'"•■i *■• 






<i^^: 



?^ 









The Parasite of Quartan Fever. 






; i. 



3Z 









35 






37 



4-1 



r 



4? 









''•Mf-^ 



PLATE 12. 



The Parasite of Aestivo Autumnal Fevei: 

34 5 



21 



22 



23 



I f 



o 



29 



30 



32 



;s 



35 



36 



U 



o 



A? 



38 



^^ 



?.f* 



39 



®^ 



€^ 



+3 



44- 






O 



"{^..-^f 



fis-. 



THE MALARIAL PARASITE. l6l 

(Plate ii). Later the arrangement of these bodies is lost and they 
are found irregularly distributed through the interior of the para- 
site. The next step appears to be the absorption or rupturing 
of the operculum, after which these bodies (sporules) are found 
disseminated through the plasma. The tertian parasite develops 
from 15 to 20 sporules, each sporule displaying a minute, faintly 
granular, dark spot at its interior — a probable nucleus. After 
the sporules are liberated, they may be seen moving about actively 
in the plasma, and later they become quiescent. At times seg- 
mentation takes place before the pigment-granules collect at 
the center of the organism. Sporulation, however, is directly 
associated with the occurrence of the chill, and is regarded as the 
asexual method for the reproduction of the parasite (Fig. 69). 

It is reasonable to suppose that the sporules, after liberation 
in the plasma, invade healthy erythrocytes, and there develop 
to the stage of sporulation, thus repeating their asexual or 
endogenous cycle. 

Quartan Parasite. — In quartan fever the parasite undergoes 
segmentation in a sHghtly different manner from that described 
in tertian fever. The pigment-granules are arranged about the 
peripher}'- of the organism, and as they near the stage of maturity 
these granules assume a stellate form extending from the periph- 
ery to the center, where a dense aggregation takes place. The 
protoplasm becomes finely granular; when true segmentation 
begins and continues as in the tertian parasite. The number 
of segments or sporules are usually from six to twelve, and the 
segmenting body is always considerably smaller than is that of 
tertian fever, and its sporules are commonly arranged to form 
perfect rosets (Plate 11). 

Estivo-autumnal Parasite. — Segmenting bodies are not com- 
monly encountered in the blood of estivo-autumnal fever, 
and it has been suggested that the asexual reproduction occurs 
in the viscera. When segmentation is to be seen, however, the 
segmenting bodies are much smaller than are either those of the 
tertian or quartan fevers, and all evidences of the red cells are 
destroyed. Crescentic, ovoid, and spheric bodies are always 
observed in the blood of estivo-autumnal fever after the infec- 
tion has existed for a period of one or more weeks (Plate 12). 
For a long period of time there has existed considerable question 
as to whether or not these bodies represented a definite stage in 
the hfe-history of the more common forms of malarial organ- 
isms. The weight of opinion, however, seems to favor the fact 
that crescentic forms are derived from pigmented intracellular 
forms. 



l62 THE BLOOD. 

Crescentic Bodies. — Crescentic bodies are rarely to be found 
within the erythrocytes. The typical crescent is a highly refrac- 
tile body from 7 to 9 [J. in length and 2 jut in breadth, exceeding 
the red corpuscle in size. Its extremities are rounded, and united 
with a dehcately curved Hne which expands the concave border 
of the crescent, and occasionally this marginal, hood-like pro- 
jection is seen extending along the convex border (Plate 12). 
Fine granules and rods of pigment are seen within the crescent, 
commonly collected about the center of its body, but occasionally 
aggregations of pigment are discernible in one of the horns. 
The pigment-granules are usually motionless, yet sHght move- 
ments may be seen where granules occupy one extremity of the 
crescent. 

Oval Bodies. — Both the oval and spheric bodies are apt to 
be smaller than are crescents, but exhibit similar features, and 
are often provided with a small hood-like questionable remnant 
of their former host, the red cell. Either oval or spheric bodies 
may be seen within the red cells (Plates 11, 12, 13). 

Extracellular Pigmented Bodies. — Certain of the extra- 
cellular bodies found in both tertian and quartan fevers do not 
undergo segmentation after they have reached maturity, but, on 
the other hand, leave their host, the red cell, and appear free in 
the blood (extracellular pigmented bodies). In their new environ- 
ment they develop rapidly, and in the tertian form may attain 
the size of a polynuclear leukocyte. The pigment-granules 
display more active movements than are to be observed under 
other conditions; the parasite becomes distorted and its outhne 
indistinct. After a time the movement of the granules gradu- 
ally lessens and finally ceases; while the body of the parasite 
becomes more and more distorted, probably resulting from its death. 

Again, certain of these organisms may show a gradual frag- 
mentation, and small particles of their pigment are seen to be 
separated from the general pigment mass. In this manner a 
parasite may be seen to divide into several smaller bodies (four 
or five); the movements of the pigment persist in the smaller 
subdivisions, but later these granules become quiescent, the body 
of the cell grows less distinct, and death ensues. At times, after 
the pigment-granules have become motionless the cell may dis- 
play vacuoles (degeneration). 

Flagella. — Generally speaking, the flagella of quartan fever 
are sHghtly smaller than are those of the tertian form (Plate 11), 
and Craig beheves that there occur in the blood of cases of 
tertian and of estivo-autumnal fevers two varieties of flagellated 
organisms. 



PLATE 13. 

Structure of the Malarial Parasite. 

Ai-ii. Tertian parasite; asexual generation: 1-9 correspond with the de- 
velopment of the organism, showing chromatin divided more and more and pro- 
gressive increase in the pigment; 10, presegmenting parasite, showing multiple 
nuclei of the future segments; 10, segmenting organism. 

B I, 2. Tertian parasite; gametes. 

C 1-5. Quartan parasite; asexual generation, showing gradation of organism 
as evidenced by age: 3, 4, maturer forms; 5, presegmenting form of the parasite. 
Note especially that the red cell is not enlarged as the result of quartan infection, 
and that the pigment is much distributed. 

D1-4. Estivo-autumnal parasite; asexual generation: i, 2, 3, early ring forms; 
4, mature parasite. 

Ei, 2, 3. Crescentic bodies: Note staining of hood-like portion of 3, which 
expands the concavity of the organism. 

F1-5. Estivo-autumnal parasite; macrogametes (ovoid bodies). 

G1-5. Estivo-autumnal parasite; microgametocytes: 4, 5, Show stained 
flagella. 

H. Blood-plates. These are often found resting upon the red cell, and are to 
be distinguished from malarial infection of such cells. 

Ii, 2. Pseudovermiculus laverania danilewskyi from crow's blood. (See Hal- 
teridium, page 155.) (Lazear in Johns Hopkins Hospital Reports, vol. x, Nos. i 
and 2.) 



PLATE 13. 



A I 



''y 



\^ 



A4 



v^^^' \ 



A5 



A6 



A? 

\ 



AS 



A9 






Aio 



An 






m¥ '%t 



Bi 






B2 



.1; 



Ci C: 



C3 



Ca Cs 






Vif' 



Di 



D2 D3 



D4 



•^ 



Ei 






^ ^^ 



^ 



E3 






F2 



F.^ 






Gi 



G2 



y^ 



G3 






G4 



Ci5 



■\ ^^ 



H 



Ii 



I2 



% 



» 



t 



THE MALARIAL PARASITE. 



163 





Method of Developing Flagella. — Ordinarily flagella make 
their appearance in from fifteen to twenty minutes after the blood 
has been withdrawn; rarely I have seen them develop sooner 
(three to ten minutes). The blood is withdrawn from the finger 
or ear (see page 33), and after removing the first few drops that 
collect at the site of puncture a drop is allowed to remain exposed 
to the air for a few seconds. Breathe upon the surface of the shde 
until it shows evidence of moisture, when 
bring the moistened surface of the sHde in 
contact with the drop of blood; add immedi- 
ately a cover-glass to that portion of the blood 
clinging to the surface of the sHde, and the 
specimen is ready for microscopic study. Flag- 
ellation is hastened by the presence of the 
moisture suppUed from breathing on the slide. 
The bodies from which flagella develop (tertian 
fever) are large and may show their pigment either in active 
movements and disseminated throughout the protoplasm (Fig. 
57, A, B), or the same pigment may be seen but a few minutes 
later occupying small blotches in the protoplasm, and practically 
motionless. 

Development of Flagella. — Certain of the extracellular 
organisms contain pigment-granules which display rapid move- 



Fig- 57- — Large body 
of tertian fever, pigment 
in blocks {A) ; B, pig- 
ment evenly dissemin- 
ated (Craig). 




Fig. 58. — A, Parasite just prior to flagel- 
lation ; B, flagellated parasite (Craig). 



Fig. 59. — Types of flagella : A, Clubbed extrem- 
ity ; B, nodular swellings; C, pigment within fla- 
gellum and at extremity ; £>, pigment at extremity ; 
£, short, thick, and pigmented (after Craig). 



ments and later collect at the center of the parasite, at which time 
the pigment becomes quiescent; while coincidentally pecuHar 
movements are to be seen along the margin of the organism. 
Almost instantaneously a protrusion or protrusions appear from 
the edge of the parasite, which elongate, forming thin, colorless, 
actively motile filaments that are seen lashing among the red cells 
(Fig. 58, A, B). The flagellum is apparently continuous with the 
border of the parasite, and may, in addition to being clubbed at 



164 



THE BLOOD. 



Fig. 60.— ^, Free flagellum 
just escaped from parasite ; 
B, shrunken state of the para- 
site after exilagellation (after 
Craig). 



its distal extremity, present one or more nodular expansions and 
a few pigment-granules (Fig. 59). In length the flagellum usually 
equals about thrice the diameter of the organism from which 
it was developed, and from four to eight times that of a red cor- 
puscle. They may be even longer, and short flagella with slug- 
gish serpentine movements may be seen. 

All flagella display an active vibratory and often whip-hke 
movement,, which displaces the red cells 
suspended in the plasma, resembhng some- 
what in this respect, yet in a lesser degree, 
the effect of the filaria upon the hving 
corpuscles. After a time the flagellum is 
detached from the body of the parasite, 
and may be seen coursing through the 
field in a more or less serpentine manner, 
traveling rather rapidly between the red 
cells. This active serpentine movement 
becomes lessened after a time, and is eventually lost, the flagellum 
often becoming entangled among the red cells. The accompany- 
ing figures (60, 61), compiled from Craig's exhaustive illustrations 
of malarial flagella developing from the various forms of malarial 
parasites,* will serve to illus- 
trate the sHght differences 
known to exist. 

Termination of Flagella. — 
(i) The flagellum may become 
detached from the parent cell; 
(2) become motionless and 
disappear; (3) coil around the 
parasite, which becomes 
shrunken and degenerated; or 
(4) the parasite may become 
fragmented and the flagellum 
degenerate and disappear. 

In the first instance, where 
the flageUum has succeeded 
in detaching itself from the 
parent cell, it swims serpent- 
like among the corpuscles (Fig. 62, 6). Should a single flagellum 
be developed from a parasite, the pigment of such parasite becomes 
quiet after the flagellum is detached, and the ceU itself soon becomes 
shrunken (Fig. 62, 7). 

In the study of flagellated malarial parasites one should observe 

* "New York Med. Jour.," Dec. 23, 1899, p. 913. 




Fig. 61. — I, Prior to flagellation; 2, parasite 
showing four flagella ; 3, fragmentation, divid- 
ing into two portions ; 4, further fragmentation ; 
5, fragmentation complete (after Craig). 



THE MALARIAL PARASITE. 



i6s 



the extreme activity of the pigment in the parasite prior to flagel- 
lation and while the flagella remain attached, also the clubbed 
extremities of the flagella (Fig. 62), as well as their power of 
individual movement in the blood. 

Passive Flagellation. — Not all cases of estivo-autumnal fever 
exhibit flagellation, since yf^ 



flagella develop from the 
crescentic bodies; yet it is 
in this form of fever that 
we commonly find the so- 
called "passive flagellated 
parasite." In addition to 
crescentic bodies there are 
also to be seen numerous 
round and oval bodies whose 
pigment is distributed in the 
form of a wreath (Figs. 63, 
64). These bodies, accord- 
ing to their pigment-gran- 
ules, are divided into two 
forms : first, those in which 
the pigment is in the form of fine rods and dots, and may at times 
be motile, again quiescent ; second, those forms which are few in 
number, nearly always round, and whose pigment is in the form of 
large, black -brown dots seldom displaying movements. The active 
flagellated organism, previously described (Fig. 61), may arise from 
the first variety, while from the second variety the passive flagel- 




Fig. 62.— Parasite of estivo-autumnal fever: i, 
Crescent within the red cell ; 2, crescent cell ex- 
panded into round body, but within the red blood- 
cell ; 3, round body which has escaped from the 
red corpuscle, which rests beside it ; 4, round body 
with active pigment ; 5, round body putting forth 
two flagella ; 6, round body showing one flagellum 
detached ; 7, shrunken and degenerated parasite 
(after Craig). 



? 



Fig. 63,— .,4, Round body with pigment 
in form of a ring ; B, pigment disseminated 
and feebly motile at times (Craig). 



Fig. 64.— A , Round bodies with pigment 
in form of a wreath ; B, oval bodies show- 
ing wreath arrangement of pigment ; C, 
round bodies with pigment in the form of 
dense aggregations (Craig). 



lated organism springs. Flagella developing from this latter variety 
of parasites are usually few in number, rarely present clubbed 
extremities, though there is an expanding portion at the junction 
of the flagellum and the mother-cell (round body), and instead 
of the active, lashing movements previously described, there is 



l66 THE BLOOD. 

to be seen a straightening, relaxing, and apparent revolving of 
the flagellum upon its axis (Fig. 65). According to Craig, they 
may detach themselves from the round body and again attach 
themselves to it. During these maneuvres the pigment-granules 
of the round parasite remain in the form of a circle, and are usu- 
ally motionless. This form of flagellation also occurs in tertian 
fever. 

Function of the Flagellum. — The flagellum represents the 
male element in the cycle of the sexual reproduction of the malarial 
parasite — flagellation takes place outside the human body and 
normally v^ithin the stomach of the mosquito. To MacCallum, 
of Baltimore, is due the discovery of the flagellum's function. 
In a manner somewhat analogous to that of the spermatozoon the 
detached flagellum penetrates a fully matured malarial parasite 
which has not yet undergone segmentation. The parasite thus 




Fig, 65. — Passive flagellation of the estivo-autumnal parasite. Note arrangement of 
pigment ; fiagella not clubbed at ends, and straight in outline. One flagellum about to enter 
round body (after Craig). 

fertihzed in the mosquito's stomach penetrates the insect's stomach- 
wall and here develops into a small cyst which in about seven days 
displays numerous irregular, ray-hke striae (see Lije-Cycle of 
Malarial Parasite, Fig. 66). Later the capsule of this cyst rup- 
tures, and the delicate, thread-Uke bodies which the cyst contains 
are hberated in the body of the mosquito, and later many of 
them are deposited in the insect's salivary glands. A mosquito 
thus infected, upon biting a healthy human being in addition to 
sucking blood from the individual, introduces into his system 
the small thread-hke bodies previously stored up in its sahvary 
glands; these bodies being the product of sexual fertihzation of 
the fully developed spermatozoon (flagellum), which fertilization 
took place in the mosquito's stomach after the insect had sati- 
ated its appetite with the blood of a person infected with malaria. 
The thread-hke bodies (Fig. 66, U), introduced into the human 
system through the mosquito's bite are now properly environed 



THE MALARIAL PARASITE. 



167 



for their further development into the hyahne bodies previously 
described. This final step completes the life-cycles of the malarial 



/V J Human Phase- [ / /] 




Fig. 66.— Schema showing the human and mosquito cycles of the malarial parasite : 
A, Normal red cell; B, C, D, E, red cells containing amebulas or myxopods ; F, G, H, 
sporocytes ; J', K', L', M', microgametocytes or male gametes; J", K", L", M", O, macro- 
gametocytes or female gametes; N', N", microgametes ; P, traveling vermicule ; Q, young 
zygote; R, S, zygotomeres ; T, blastophore ; U, mature zygote (modified from Blanchard's 
diagram illustrating life-cycle of Coccidium schubergi) (Rees, in " Practitioner," March, 1901). 



parasite in both its host — man — and the intermediary host — the 
mosquito. More than one variety of parasite may be found in 
the blood of man at the same time. 

For a description of the Leishman-Donovan body see p. 525. 



CHAPTER II. 
THE URINE. 

It is of utmost importance that the physician have an extensive 
knowledge of this secretion, since its many variable changes are 
often expressions of morbid conditions in either the kidneys them- 
selves or elsev^here in the body; an accurate interpretation of 
these changes provides valuable aid to diagnosis; therefore 
the study of the urine has now become one of the essential fea- 
tures in clinical diagnosis. 

PHYSICAL PROPERTIES OF THE URINE. 

NAKED-EYE APPEARANCE. 

Quantity. — The quantity of urine secreted by a healthy man 
in twenty-four hours is from 1500 to 2000 c.c. (42.2 to 52.7 fl. 
oz.); although 1200 c.c. (33.8 fl. oz.) may at times be the normal 
quantity where but few liquids are taken. Marked variations 
are commonly observed, and, as a rule, bear direct relation to 
the quantity of fluids taken, and the activity of the bowels or 
the skin; therefore, any excess or deficiency in this quantity 
secreted should be regarded as pathologic only when extreme. 
The rate of secretion varies with barometric conditions (tempera- 
ture and humidity), and is increased during the early part of 
the night and early morning; while during the hours usually 
occupied for sleep and during sleep it is lessened. 

Under pathologic conditions we often observe wide deviations 
from the normal standard, and in order to arrive at definite con- 
clusions the urine voided during the twenty-four hours should be 
collected. The patient should void all the urine possible before 
going to stool, thus diminishing loss during the act of defecation. 
When the patient suffers from incontinence, the quantity is 
approximately estimated by frequent catheterization; yet this 
procedure is open to many objections, as is also the permanent 
application of a catheter. Care must be taken to empty the 
bladder before any of the urine for the twenty-four hours is col- 
lected. Collect the urine in a graduated vessel of 2000 c.c. (52.7 

168 



NAKED-EYE APPEARANCE. 169 

fl. oz.) capacity, in order that the quantity may be estimated. 
When further study is desired, keep the urine in a cool place to 
prevent decomposition, which is destructive to many of its ele- 
ments. 

Oliguria. — A diminution in the quantity of the urine se- 
creted is a feature accompanying high fevers, interference v^ith 
the renal circulation, — as in chronic heart disease, — cirrhosis of 
the liver, hydroperitoneum, and acute and certain forms of chronic 
nephritis. 

Anuria. — Complete suppression of the urine may accompany 
uremia and conditions where large quantities of liquids are 
extracted from the body: e. g., Asiatic cholera, dysentery, hemor- 
rhage, and grave anemia. It also follows the administration of 
large doses of arsenic and oxahc acid (toxic anuria). Suppres- 
sion of the urine may follow profuse perspiration (physiologic 
anuria) . 

Polyuria. — A notable increase in the quantity of the urine 
is observed in chronic interstitial nephritis, amyloid disease of 
the kidneys, during the convalescence from acute nephritis, acute 
fevers, and in diabetes mellitus and insipidus. It is also present 
after hysteric seizures and in certain organic brain conditions; 
in cardiac disease after compensation is re-established; during 
the absorption of fluids from the serous sacs; and between the 
paroxysms of relapsing fever. It may also follow the adminis- 
tration of drugs; e. g., digitalis and caffein. 

Color. — Normal urine is of a straw or wine-yellow color. 
Marked variations from the normal are seen, extending from that 
of a clear watery urine, of low specific gravity, containing little 
coloring pigment and a comparatively small quantity of solids, 
through the successive shades to that of a reddish-brown urine, 
of high specific gravity, rich in both coloring-matter and solids. 
The pigments usually regarded as accountable for the color of 
the urine are uroerythrin, pigment of pink urates, normal urobilin, 
pathologic urobilin, — present during seizures of pyrexia and in 
grave anemia, — urohematoporphyrin (derivative of hematin), 
and alkapton, the color of which appears after exposure to air and 
light. The reaction exercises an influence upon the color of 
the urine; e. g., acid urines are, as a rule, darker than are alkaline 
urines, and should an acid reaction persist, the color of the urine 
deepens upon standing. 

Normal urine is of a golden- or amber-yellow color, while 
highly colored urines may vary through the successive shades to a 
reddish yellow or red color, and dark urines from brownish red 
to reddish brown. 



lyo THE URINE. 

Color in Disease. — Pathologic urine may present a pale color 
and high specific gravity, or vice versa. Here the color of the 
urine may depend upon the secretion of additional coloring- 
matter. Wide variations, depending on the stage of the disease 
at which the urine is examined, are to be observed; e. g., the urine 
secreted on the second day of an attack of acute nephritis is of 
high color, scanty, and of high specific gravity; while the urine 
at the beginning of convalescence is pale, increased in quantity, 
and of a low specific gravity. 

Highly colored urine is noted in fevers, conditions causing 
congestion of the kidneys — as in chronic heart disease, pernicious 
anemia, sarcoma, and cancer of the gastro-intestinal tract. Prod- 
ucts of pathologic urobilin, indigo, melanin, or anemia, when 
contained in the urine in sufficient amounts, may, on the addition 
of some reagent, develop color. On standing, the urine of phthisis 
has a tendency to become dark, and, at times, black. Such 
changes are often due to the development of fungi, and are pro- 
duced experimentally by the Aspergillus fumigatus and A. niger. 

Polyuria. — Polyuria resulting from diabetes insipidus and 
interstitial or amyloid changes in the kidneys follows the usual 
rule of diminished pigments and solids; while, on the contrary, 
the urine of diabetes mellitus is of high specific gravity and as a 
rule of an amber color. 

Chyluria. — Chyluria, parasitic or from other cause, lends to 
the urine a milky appearance due to the addition of globules of 
fat. 

Bloody Urine. — Urine of a reddish, carmin, or blackish 
color usually contains an admixture of blood, and varies in color 
proportionate to the quantity added. Bile-pigment lends to the 
urine a brownish-yellow color, and if present in large amounts a 
greenish tint is observed: on shaking, a heavy yellow foam 
collects on the surface. Urine rich in urobilin is brownish red 
in color and may on shaking also display a froth. Indoxyl 
sulphate may cause a dark-brown hue. Indigo is responsible 
for the blue or dull blue color in the urine. 

Green Urine and Drugs. — Green urine is rarely seen and may 
be due to the presence of biliary coloring-matter (greenish yellow 
or greenish brown); to large amounts of sugar, cystin, develop- 
ment of bacteria (Bacillus pyocyaneus), and to the administra- 
tion of methylene-blue. The latter is a common cause of bottle- 
green urines in the insane department of the Philadelphia Hos- 
pital, where the drug is employed as a sedative. CarboHc acid 
induces a brown color which on standing changes to a blackish 
brown; a similar effect being produced by naphthalin, resorcin, 



NAKED-EYE APPEARANCE. 



171 



hydroquinon, and pyrocatechin. Rhubarb and senna cause a 
brown or red color, while santonin induces a yellow tint; quinin, 
antipyrin, and sulphonal intensify the color of the urine. The 
coloring pigments of the urine are doubtless many in number, 
among which hematoporphyrin is seen. 




Fig. 67.— Urine turbid, due to urates. Upper stratum heated. 



Transparency. — Normal urine is clear when voided, and 
upon standing it usually becomes cloudy, but is not affected by 
alkalis, mineral acids, or by heat. Pathologic urine may be 
cloudy when voided, or may become so, owing to precipitation of 
urates, phosphates, carbonates, blood, pus, mucus, chyle, or 
bacteria. Turbidity due to phosphates clears by the addition 



172 THE URINE. 

of acids, and that induced by urates, by the apphcation of heat 
(Fig. 67). Should the turbidity increase when acid and heat are 
apphed, it is due to albuminous products or to earthy phosphates 
(see Scheme, page 261). Turbidity due to mucus or bacteria 
is but moderately influenced by acetic acid. 

Odor. — The odor of fresh normal urine is that of new hay; 
decomposition causes the odor of ammonia. Urine containing 
acetone has an odor of fruit; while that of diabetes gives an 
aromatic odor. Asparagus, onions, and turpentine in turn lend 
their characteristic odors to this secretion. Blood when in alka- 
line urine induces a heavy, putrid odor. 

Consistence. — Normal urine is of an aqueous consistence. 
Urine is thickened by large amounts of sugar, mucus (syrupy), 
pus, molecular fats, Bence- Jones' albumose, and also, in certain 
febrile conditions, as the result of an excess of inorganic sub- 
stances. Alkalinity may also increase the consistence, this con- 
sistence being rarely found to be that of gelatin. 



SPECIFIC GRAVITY. 

The standard for normal urine, when the entire quantity 
has been collected for the twenty-four hours, can safely be set 
at 1.020. It usually varies in inverse ratio to the quantity secreted, 
oscillating between 1.015 and 1.025 when 1200 to 1500 c.c. 
(33.8 to 42.2 fl. oz.) are voided daily. 

Increase. — Nitrogenous foods, fasting, sedentary habits, and 
pathologic states cause increase; while the taking of large quan- 
tities of liquid into the system diminishes the specific gravity. 

Urines rich in urates, chlorids, phosphates, oxalates, and 
sugar display a high specific gravity. An increase is also ob- 
served where the quantity of urine passed is lessened; e. g., in 
acute fevers, acute and chronic nephritis, after mineral poisons, 
eclampsia, uremia, and following a dry and highly albuminous 
diet. 

Caution. — The specific gravity bears no relation to the 
nitrogenous constituents of the urine, yet increased nitrogenous 
elimination and an increased elimination of chlorids are commonly 
associated, the latter inducing a high specific gravity. 

Decrease. — A marked diminution in the specific gravity of 
the urine may be the first evidence that the kidneys are incapable 
of performing their function. In chronic nephritis a diminished 
specific gravity often precedes an attack of uremia; yet the quan- 
tity of urine secreted may be normal or even increased. In 
diabetes insipidus, amyloid kidney, chronic interstitial nephritis. 



SPECIFIC GRAVITY. 



173 



19. 



and after the excessive inhibition of malt Hquors, the specific 
gravity is lowered. I found it to be 1.004 in Bence- Jones' albu- 
mosuria, a condition where a low specific gravity is common. 

In acute fevers where the specific gravity has been high, a 
sudden diminution signifies either that tissue changes are dimin- 
ished, their products not formed, or that those processes are active 
and their products not elaborated by the kidneys; however, it 
may be the first evidence of a fatal termination. A series of cases 
studied at the Philadelphia Hospital showed that in acute fevers, 
chronic nephritis, and in acute alcohohsm, a marked lessening 
in the specific gravity, without change in quantity of the urine, 
often preceded severe nervous symptoms, which were frequently 
accompanied by oliguria. 

Estimation of the specific gravity is readily obtained by the 
use of the urinometer (Fig. 68), which 
should always be furnished with a 
thermometer, as such instruments are 
standardized at a given temperature. 
(For every seven degrees above the 
temperature at which the urinometer 
is standardized add one degree to the 
specific gravity.) 

Method. — Fill a cylindric graduate 
(Fig. 68) two-thirds full of urine, and 
remove all froth by touching to it a 
slip of filter-paper. Introduce the 
urinometer into the graduate and 
gently force it to sink to near the 
bottom of the fluid, when it will be 
seen to rise and fall until it seeks its 

level. The figure at the surface of the urine represents the 
specific gravity of the specimen under examination. Should the 
quantity of urine be too small for determination of its specific 
gravity by the urinometer, place the urine at hand in a small 
cylinder and proceed in the determination by means of "specific 
gravity beads" (Fig. 69), which are graduated from 1.002 to 1.050. 
Allow several of the beads to fall gently into the urine and read 
the specific gravity from the surface of the bead that remains 
suspended at the center of the column of urine (Fig. 69). 

Caution. — The beads should be kept in clear water and 
cleansed by changing this water after their use. The use of the 
pyknometer, while insuring accuracy, is not practical for daily 
chnical work. 

Pathologic urine may vary from 1.002 to 1.045 ^^^" even higher. 




Fig. 68. — Squibb's urinometer. 



174 



THE URINE. 



The specific gravity of the urine is of importance, since it bears 
an approximate relation to the metabohc changes; however, 
where the kidneys' function is impaired, products resulting from 
metabohc changes, as uric acid and urea, may be formed in normal 
amounts and still be retained in the blood and tissues, thereby 
diminishing the urine's specific gravity. 

Solids of the Urine. — The quantity of solids excreted through 
the urine in a healthy individual of average weight and habits 



i 






\ 



Fig. 69. — Use of beads for determining the specific gravity of small quantities of urine and 

other fluids. 



during the twenty-four hours is estimated at 945 grains (61.14 
gm.). After the fortieth year the amount of solids will be found 
to diminish gradually; and to meet this reduction deduct 10 per 
cent, from the above standard during the decad between forty 
and fifty; and an additional 10 per cent, for each successive 
decad. Conditions altering the amount of solids excreted are 
largely those influencing the specific gravity of the urine. 

Computation. — The total amount of solids is estimated by 
multiplying the last two figures of the specific gravity by 2.33,, 



ELECTRIC CONDUCTIVITY OF THE URINE. 1 75 

the co-efficient of Haeser; e. g., the urine voided during the twenty- 
four hours is found to be 1800 c.c, and the mixed product has a 
specific gravity of 1.020. Therefore 20 X 2.33 = 46.60, the amount 
of sohds estimated in grams present in 1000 c.c, of such urine, and 
4 . o X I 00 ^ g^ g^ ^YiQ number of grams of sohds suspended in the 

urine voided during the twenty-four hours. The cHnical value of 
estimating the total amount of sohds has certain limitations, for 
which reason more elaborate methods are omitted (see Chemistry, 
page 177). It should be emphasized that the determination 
of the total solids of a given specimen voided at one urination 
is valueless, since the specific gravity fluctuates between wide 
limits at different hours of the day. 

ELECTRIC CONDUCTIVITY OF THE URINE, 

Electric conductivity of the urine in relation to its chemic 
composition is among the newer applications of modern physio- 
logic chemistry, and is of importance when employed in the solu- 
tion of problems in both physiology and physiologic chemistry. 
It is fair to beheve that it will add greatly to our present 
laboratory methods for the ascertainment of pathologic states of 
the urine. (Electric conductivity may also be applied to other 
body fluids — pleural and peritoneal. It has been shown by 
Roth,* Stewart, t Bugarszky,J Tangl,§ and a number of other 
observers that this method is applicable to the examination of 
both blood- serum and serous fluids. They have further found 
that the inorganic constituents of blood-serum are much more 
constant than are the inorganic constituents of urine.) The 
extended variations in the conductivity of urine cause one at first 
sight to regard them as being of little clinical moment. Bugar- 
szkyll has shown that certain general relations exist between the 
total ash of the urine and the conductivity, showing that the con- 
ductivity of the urine is practically due to the mineral salts held 
in suspension. 

Urea. — Most abundant of the urinary constituents is the urea, 
which is nearly a non-conductor when thus suspended in solution, 
and it does not, therefore, materially influence our results. Kreat- 
inin, ammonia, xanthin bases, uric acid, and urates have but 
slight conductivity. The conductivity of the urine and the 
specific gravity when studied correlatively will be found to have 
a value somewhat analogous, the former being slightly the more 

*"Centralbl. f. Physiologic," Nov. 27, 1S97. 

"l Ibid., p. 332. t Ibid., p. 2Q7. § Ibid., p. 301. 

II "Pfliiger's Archiv f. die gesammte Physiologic," 1897, vol. Ixviii, p. 3S9. 



176 THE URINE. 

definite, which renders electric conductivity of value in estimating 
the degree of metabolism of inorganic substances — a point v^hich 
has been ably demonstrated by J. H. Long*- who has also elab- 
orately described the special technic necessary for the applica- 
tion of this method, as have also other writers to whom I have 
referred. 

REACTION OF THE URINE. 

Healthy mixed urine from the twenty-four hours' product is 
acid, due to the presence of diacid sodium phosphate (NaH2P0J. 
Such acids as uric, sulphuric, carbonic, and hippuric are thought 
to take up a portion of the sodium from the urine, leaving behind 
an acid salt. Taylor estimated the acidity of the normal urine 
for twenty-four hours as equivalent to 14 grains of carbonate of 
sodium or 30 grains of oxalic acid. 

Decreased Acidity. — Conditions lessening the degree of 
acidity are a full meal, a diet largely vegetable, ingestion of foods 
rich in vegetable acids or their salts, such as acetates, lactates, 
and tartrates, alkaline carbonates, free perspiration, and parox- 
ysms of vomiting. Temporarily diminished acidity is observed in 
pneumonia during the forenoon (Quincke) and twenty-four hours 
after the crisis. Standing lessens the acidity through decomposi- 
tion of the urate of sodium. 

Increased Acidity. — The acidity is increased by allowing the 
urine to stand for a few hours, and is due to an increase of lactic 
and acetic acids, acid phosphates, and probably to the formation 
of new acids from such pre-existing substances as alcohol and 
carbohydrates (diabetic urines). This acid stage is of short dura- 
tion and the urine is rendered alkaline by the action of bacteria, 
as well as by chemic changes. Muscular exercise, a diet largely 
of meats, and the taking of mineral acids increase the urine's 
acidity, and high acidity is a feature of acute fevers, scurvy, 
phthisis, diabetes, and leukemia. 

Alkaline Reaction. — Pathologic urine may be alkahne when 
voided, due to ammoniacal fermentation of uric acid and the 
breaking- up of urea into ammonium carbonate. Thus : 

Urea water ammonium 

carbonate. 

Such a condition implies that there are pathologic changes along 
the urinary tract, commonly the bladder. 

Method of Detecting Reaction. — The reaction of urine 

* "Jour, of the Amer. Chem. Soc," Oct., 1902, vol. xxiv, No. 10. 



CHEMISTRY OF THE URINE. 1 77 

is taken by means of red and blue litmus- papers, blue litmus being 
turned red by acid urines, while alkaline urines change red litmus 
to blue. The litmus should be cut into narrow strips and kept 
in a well-stoppered glass jar. Immerse the slip in water im- 
mediately before use and then dip one-half inch of its tip into 
the urine, when the change induced by the urine will appear. 

Amphoteric Reaction. — The same urine may at times 
change red litmus to blue and blue Htmus to red (amphoteric). 
This peculiar reaction depends upon the presence of both acids 
and neutral sodium phosphates, which substances are eliminated 
simultaneously and equally. 

Fixed and Volatile Alkalis. — To distinguish between alka- 
linity due to fixed alkali (sodium or potassium) and that due 
to a volatile alkali (ammonia), red litmus-paper, which has been 
turned blue by the alkalinity of the urine, is dried by gentle heat. 
No change is observed when a fixed alkali is present, but if the 
alkalinity depends upon a volatile alkali (ammonia), the litmus 
surrenders its blue color and displays a reddish or yellow tint. 



CHEMISTRY OF THE URINE, 

The exact chemic composition of the urine is by no means 
constant, but fluctuates within rather wide limitations even in 
the apparently normal individual; and these variations depend, 
in great measure, upon such factors as exercise, age, sex, cold or 
hot baths, diet, temperature, digestion, and sleep. A fair classi- 
fication of the constituents of healthy urine has been suggested 
by Parkes and is shown by the following table : 



Constituents. Weight, 66 Kilogi 

Water 1500.00 g 

Total solids 72.00 

Urea 33.18 

Uric acid 0.55 

Hippuric acid 0.40 

Kreatinin 0.91 

Pigment and other organic 

matters 10.00 

Sulphuric acid 2.01 

Phosphoric acid 3.16 

Chlorin 7-8.00 

Ammonia .' 0.77 

Potassium 2.50 

Sodium 11.09 

Calcium 0.26 

Magnesium 0.2 1 

12 



Per Kilogram 
Body-weight. 


22.730 
1.090 
0.500 


gm. 


0.008 
0.006 




0.014 




0.15 1 




0.030 
0.048 
0.126 





iy8 THE URINE. 

Becquerel's estimation for each looo grains of urine is, water 
967 grains; solids 33 grains. Of the sohds, 24.865 grains were 
organic matter, leaving but 8.135 grains of inorganic substance. 

During certain pathologic conditions the urine may hold in 
solution, in variable amounts, many substances, among which are: 
serum- albumin, serum-globulin, peptone, albumose (Bence- Jones'), 
nucleo-albumin (mucin), glucose, dextrin, lactose, inosite, 
blood-pigments, bile-pigments and bile acids, melanin, leucin, 
tyrosin, oxybutyric acid, lecithin, allantoin, fat, acetone, choles- 
terin, urocaninic acid, sulphureted hydrogen, cystin, and alcohol. 



MINERAL ASH, 

Quantitative Estimation. — i. Fifty c.c. of urine are placed 
in a porcelain dish, the weight of which has been taken. It is 
then evaporated to dryness at a temperature of 100° C. Heat 
until no gas is evolved. 

2. The residue is now taken up by distilled boiling water and 
later filtered through a filter the weight 
of whose ash is known. 

3. Both dish and contents of the filter 
are washed with hot water, and the dish 
and filter dried in an oven; after which 
the filter is placed in the dish and slowly 
incinerated. 

4. When the dish becomes white, the 
washings and filtrate which have been set 
aside are now added to the ash and evapor- 

Fig. 7o.-Desiccator. ^^cd at ioo° C. Prolong the heat over the 

flame — care being taken lest too great heat 

be applied and certain substances be volatilized (chlorin), and 

sulphates converted into sulphids in the presence of organic 

matter. 

5. Cool the dish in a desiccator (Fig. 70) and ascertain its 
weight. The difference between its present and previous weights 
equals the quantity of ash in 50 c.c. of urine. 

Cautions. — Place 4 to 6 ounces of dried desiccated (lump) 
calcium chlorid in the bottom of the desiccator. This keeps 
the interior of the jar dry and absorbs any moisture present. 
The lid of the desiccator is ground to fit the jar, and should 
be hermetically sealed by smearing the edge (ground surface) 
of the Hd with equal parts of paraffin and vasehn. A desic- 
cator provided with a special shelf for the calcium may be 
obtained. 




CHLORIDS. 179 

CHLORIDS. 

Chief of the alkahs found in the urine is sodium in com- 
bination with chlorin, 10 to 15 gm. being excreted by a healthy 
man during twenty-four hours. Chlorin in combination with cal- 
cium, magnesium, potassium, and ammonium is found in small 
proportions. In health, the amount of sodium chlorid excreted is 
directly influenced by the quantity and quality of food ingested. 

Decrease. — The chlorids are decreased in starvation, and 
temporarily after taking freely of liquids, in certain febrile con- 
ditions, notably typhoid fever, scarlet fever, roseola, variola, 
typhus fever, acute yellow atrophy, and they may be absent in 
croupous pneumonia. A correspondingly marked decrease is 
seen in acute and chronic nephritis when associated with albu- 
minuria; also in chronic lead intoxication, pemphigus, impetigo, 
and the early stage of dementia. Again, it is visible in chronic 
gastro-intestinal conditions, as gastric ulcer, cancer, dilatation of 
the stomach, and in diarrhea. A less marked decrease is noticed 
in the anemias, rickets, chorea, idiocy, and melancholia. 

Increase. — The chlorids are increased after the administration 
of potassium salts, during the absorption of exudates and trans- 
udates, following epileptic seizures (polyuria), diabetes insipidus, 
when they have been retained in acute febrile conditions, and 
during and immediately after the paroxysm in intermittent fever. 

Detection of Chlorids. — Reagents Required. — i. Nitric acid. 
2. Solution of silver nitrate (i dram of the crystalline salt to 
the ounce). 

The above solution of nitrate of silver, when added to albumin- 
free urine, is capable of precipitating the chlorids where the urine 
is first acidulated by adding a few drops of nitric acid. This 
precipitate appears as an opaque, milky- white chlorid of silver. 
Normal urine contains from J to i per cent, of chlorids. 

Application. — i. Ten to 15 c.c. of urine free from albumin 
(see Albumin^ page 206) are placed in a test-tube, and to it a few 
drops of nitric acid are added, the tube being then shaken. 

2. Add, drop by drop, the silver solution, noting carefully 
any changes that occur. 

Each drop of the silver solution causes a curdy, white clump 
to fall to the bottom of the tube, this mass in normal urine not 
becoming disseminated upon shaking the tube, nor does it tend 
to make the entire liquid milky. 

Should the chlorids be reduced to o.i per cent., the drop 
of silver solution merely causes an opalescence; while in the 
absence of chlorids no change is observed. A copious precipitate 



l8o THE URINE. 

is indicative of an increase in the quantity of chlorids present. 
The precipitate due to chlorids is soluble in ammonia, but in- 
soluble in nitric acid. 

Quantitative Estimation of the Chlorids. — Salkowski^s 
Modification of Volhard's Method. — Reagents Required. — i. Pure 
nitric acid, specific gravity 1.2. 

2. Concentrated solution of double sulphate of iron and am- 
monia free from chlorin (may be freed from chlorin by recrystal- 
lization). 

3. Saturated solution of nitrate of silver (29.075 gm. to the 
liter); i c.c. of such solution corresponds to o.oi gm. of sodium 
chlorid. The crystallized salt should be employed. 

4. Sulphocyanid of potassium or of ammonium dissolved 
in water 6|- gm., adding water sufficient to make 400 c.c. 
(2.5 c.c. of this solution correspond to 10 c.c. of the standard 
silver solution). 

The following method may be employed for standardizing 
the sulphocyanid solution: 

Ten c.c. of silver solution (3) are placed in a flask and 90 c.c. 
of water added. Four c.c. of nitric acid (i) are now added; 
and finally 5 c.c. of the double sulphate solution (2). After the 
mixture is well shaken, the sulphocyanid of ammonium solution 
is carefully added from the buret until a slight red color appears. 
This process should be repeated often, noting at each time the 
quantity of sulphocyanid solution necessary, and the mean ob- 
tained. Based upon these results the sulphocyanid solution is 
diluted to a point so that 2.5 c.c. correspond to i.o c.c. of the 
silver solution. Should the reaction (red color) appear after 20 
c.c. of the sulphocyanid solution are added, the following formula 
serves to determine the quantity of water to be added to one liter 
— 20 : 25 :: 1000 -.x {x equals 1250), therefore 250 c.c. of water 
are added in order that 25 c.c. shall correspond to 10 c.c. of the 
silver solution. 

Application. — i. Ten c.c. of the urine previously freed from 
albumin are placed in a flask of 100 c.c. capacity. 

2. Add 50 c.c. of water. 

3. Then add 4 c.c. of the nitric acid (i) and follow with an 
excess (15 c.c.) of the silver nitrate (3). 

4. The mixture is now vigorously shaken until the precipita- 
tion is completed and the fluid begins to clear, when enough water 
is added to make 100 c.c. 

5. Filter through a dry paper into a flask holding 80 c.c. ■ 

6. These 80 c.c. of fluid are now transferred to a flask of 250 
c.c. capacity. 



PHOSPHATES. 



l8l 



7. Five c.c. of the solution of the double sulphate of iron and 
ammonia (2) are added. 

8. The sulphocyanid solution of ammonia (4), 25 c.c. of which 
equal 10 c.c. of silver nitrate (3), is slowly added from the buret 
(Fig. 71) until the terminal reaction (a red color) is obtained and does 
not disappear on shaking. 

The excess of silver solution not needed to precipitate the 
chlorids from 10 c.c. of urine is now estimated volumetrically 
by the sulphocyanid of ammonium solution, 2.5 c.c. of which 
correspond to i.o c.c. of the silver solution: There- 
fore should 12.5 c.c. of sulphocyanid solution be 
required to produce the terminal reaction, then 
there were 5 c.c. of the silver solution not employed 
in precipitating the chlorids from the 10 c.c. of 
urine. Since 15 c.c. of silver solution were added 
and 5 c.c. were found to be in excess, it required 
10 c.c. to precipitate the chlorids from 10 c.c. of 
urine. 

Again: i c.c. of silver solution corresponds 
to o.oi gm. of sodium chlorid, and since 10 c.c. 
of silver solution have been required, o.i gm. of 
sodium chlorid being present in the 10 c.c. of 
urine, 100 c.c. would therefore contain i.o gm. 
Judging, for example, the twenty-four hours' pro- 
duct to have equaled 800 c.c, there would there- 
fore have been excreted during the twenty-four 
hours 8 gm. of sodium chlorid. 

PHOSPHATES. 

Under normal conditions the urine of the 
twenty-four hours' product will be found to con- pj^ 7i._one-hun- 
tain from 2.5 to 3.5 gm. of phosphoric acid. This died c.c. buret. 
is derived in most part from the food; a small 
portion is referable, however, to that stored up in proteid mole- 
cules in the nerve- cells, muscle- cells, red blood- cells, and the 
bones. Nerve tissue which is rich in lecithin and in nucleins 
yields much phosphorus, which is found both in combination with 
the aikahne earths (earthy phosphates) and with the alkalis 
(alkaline phosphates). Of these, the alkaline phosphates are in 
excess by one-third. Sodium enters into combination with the 
greater portion of the phosphoric acid, potassium, calcium, and 
magnesium salts in a small amount, and glycerin as glycerin- 
phosphoric acid only in a trace. 



l82 THE URINE. 

Earthy Phosphates. — Earthy phosphates are phosphates of 
calcium and of magnesium and exist in the proportion of 33 to 
67. There are from i.o to 1.5 gm. excreted during the twenty- 
four hours. They are insoluble in water, but soluble in acids, 
and are held in solution in acid urines; while in urines alkahne 
the result of fermentative changes, ammonia is set free by the de- 
composition of urea, and unites with the acid magnesium phosphates, 
forming characteristic crystals (triple phosphates). (Fig. 106.) 

Caution. — Do not mistake the precipitate which forms upon 
the application of heat to such urines for that of serum-albumin, 
which it closely resembles, nor for clouding the result of inflam- 
matory exudates from the urethra or bladder. The opacity caused 
by phosphates clears upon the addition of acids. 

Alkaline Phosphates. — Alkaline phosphates consist of the 
acid phosphates of sodium and phosphates of potassium — the 
former being abundant, the latter scant. They are freely soluble 
in water and in alkalis. Two to 4 gm. are excreted during 
the twenty-four hours. The acidity of the urine depends upon 
the quantity of diacid sodium phosphate (NaH2P0J present. 
This salt also helps to hold in solution the calcium phosphates of 
acid urines. 

As has been previously stated of chlorids, the phosphates are 
increased by the ingestion of large quantities of Hquids, food, 
animal diet, during starvation and increased tissue destruction, 
reaching the maximum toward evening, falling gradually, and 
reaching the minimum about midnight. Morbid conditions may 
cause either an increase or a diminution in the total amount of 
phosphates. 

Increase. — An increase is noted in leukemia, convalescence 
from acute fevers, diabetes insipidus, diabetes melhtus (phos- 
phates appearing in inverse ratio to the quantity of sugar), and 
during the febrile stage of cerebrospinal meningitis, mania (stage 
of excitement), tabes dorsalis, cerebral tumor, and arthritis de- 
formans. 

Drugs. — Such drugs as are cerebral depressants, maximum 
doses of alcohol, morphin, chloral, chloroform, mineral and 
vegetable acids, and potassium bromid, also cause an increased 
elimination, as do hot baths and exposure to a low temperature. 

Diabetes. — Phosphatic diabetes has at times been used to 
distinguish an increased elimination of phosphates reaching a 
maximum of 9 gm. during the twenty-four hours, and associated 
with many of the symptoms of diabetes mellitus. Sugar is rarely 
present. 

Decrease. — Phosphates are diminished in acute fevers, — 



PHOSPHATES. 183 

probably due to retention, — being most marked prior to death; 
likewise in chronic nephritis, amyloid kidney, anemias, Addison's 
disease, osteomalacia, major hysteria, chronic rheumatism, acute 
rheumatism, chronic lead intoxication, acute yellow atrophy, 
hepatic cirrhosis, and in many of the chronic nervous dis- 
eases (hydrocephalus, progressive paralysis, cerebral syphilis). 
In mania (stage of depression) and in melancholia the alkaline 
phosphates diminish, while the earthy phosphates increase. 

Drugs and Baths. — Certain drugs, as quinin and cocain, are 
followed by a decrease; while a relative decrease follows the use 
of strychnin, alcohol, valerian, phosphoric acid, cold baths, and 
sea-bathing. 

Detection of Earthy Phosphates. — Render 10 c.c. of urine 
alkahne by adding either caustic soda, potash, or ammonia; 
heat gently, when the phosphates will be precipitated as a whitish 
cloud which collects at the bottom of the tube. This precipi- 
tate is soluble in acetic acid. 

Estimation of Earthy Phosphates (Approximate). — Ultz- 
mann's Method. — A special graduated test-tube two centimeters 
wide is required. 

1. This tube is filled v/ith urine to a depth of 5.33 cm. 

2. Add a few^ drops of ammonium or potassium hydrate, and 
apply heat gently, when the earthy phosphates are precipitated. 

3. The tube is allowed to stand for fifteen to twenty minutes, 
and the depth of the sediment as registered by the tube is taken. 
A depth of from i to ij centimeters equals the normal amount. 
Should the sediment register above or below these points, there 
is either an increase or a decrease in the earthy phosphates. 

Most urines which are alkahne as the result of decomposition 
display a heavy sediment of earthy phosphates. 

Caution. — Do not mistake such sediment for an excess of phos- 
phates, as it is frequently seen in urine deficient in earthy phos- 
phates. 

Clinical Significance. — Earthy phosphates are increased 
in* osteomalacia, rickets, rheumatoid arthritis, cerebral disorders, 
mental strain, and by food and drink. A decrease is observed 
in renal disease. 

Detection and Estimation of Alkaline Phosphates (Ap- 
proximate). — Reagent. — Magnesium fluid (magnesium sulphate 
and ammonium chlorid, each, i part; distilled water, 8 parts; 
pure Hquor ammonia, i part). 

Earthy phosphates are precipitated by ammonia and readily 
removed by filtration; but since their clinical importance is Hmited, 
-their removal is not always required. 



1 84 



THE URINE. 



Application. — i. Fifty c.c. of the urine are placed in a test- 
glass and to it 5 c.c. of the magnesium solution are added, shaking 
gently. 

2. A snowy deposit of crystalline ammoniomagnesium phos- 
phate and of amorphous calcium phosphate appears. Should the 
entire liquid have the appearance of milk, the alkaline phos- 
phates are normal in amount; the appearance of cream indicating 
an excess, while a faint cloud or opalescence is indicative of a 
decrease. 

Clinical Significance. — The reader is referred to general re- 
marks, page 181. 

Estimation of Phosphoric Acid. — Reagents. — i. Acetate of 
soda solution (100 gm. of acetate of soda are dissolved in 800 c.c. 
of distilled water; 100 c.c. of a 30 per cent, solution of acetic 

acid are added, and enough distilled 
water to make 1000 c.c). 

2. Potassium ferrocyanid (saturated 
solution), or cochineal tincture (a few 
grams of cochineal in a 25 per cent, 
solution of alcohol). 

3. Uranium solution (take 20.3 gm. 
of commercial uranium nitrate, purified 
and well dried, and dissolve in a small 
quantity of acetic or nitric acid; add 
distilled water to make i liter). One c.c. 
indicates 5 mgm. of P2O5. 

Application. — i. Fifty c.c. of urine 
are placed in a beaker (Fig. 72) and 5 c.c. of soda solution (i) 
added. 

2. A few drops of the cochineal tincture (2) are now added, and 
the mixture heated vigorously over a water-bath. 

3. The uranium solution (3) is now gradually added from 
a buret until a slight, but permanent, green color is established. 

The terminal or color reaction develops after all the phosphoric 
acid has been precipitated by the uranium solution. When 
ferrocyanid of potassium is used as the indicator, a reddish-brown 
color appears. Whenever the precipitate ceases to form, the ad- 
dition of the uranium solution is suspended, the mixture stirred, 
and a drop placed on a porcelain dish, and to it a drop of fer- 
rocyanid solution added. Should no reddish-brown color appear 
at the point of contact, the uranium solution and heat are con- 
tinued. 

The number of cubic centimeters of uranium solution em- 
ployed w^hen multiplied by 0.005 equals the amount of phosphoric 




Nest of beakers. 



SULPHATES. 185 

acid contained in the 50 c.c. of urine. From this result the quan- 
tity ehminated for the twenty-four hours is readily calculated. 



SULPHATES. 

Sulphuric acid exists in the urine both as mineral (preformed) 
sulphates and as ethereal (conjugate) sulphates. In a healthy 
individual the total excretion of sulphates through the urine for the 
twenty-four hours varies from 2 to 3 gm. — less than one- tenth of 
which is ethereal sulphates. The quantity of sulphates excreted is 
greatly influenced both by the amount of proteid substance ingested 
and by the rapid destruction of the tissues. 

Increase. — ^An increased elimination is observed after a 
diet of animal proteids, in acute fevers, pneumonia, myehtis, 
cerebritis, rheumatism, affections of the muscles, and especially 
in meningitis. In diabetes mellitus, diabetes insipidus, eczema, 
pseudohypertrophic paralysis, progressive muscular atrophy, and 
leukemia, an increase appears and is especially marked i'n the 
latter condition. 

Drugs. — Morphin, potassium bromid, sodium salicylate, and 
antifebrin also cause an increased elimination. 

Ethereal Sulphates. — Ethereal or conjugate sulphates are 
found increased during certain pathologic conditions associated 
with diminished hydrochloric acid; hence intestinal fermenta- 
tion; obstructive jaundice and intestinal obstruction cause an 
increase. The normal ratio of mineral to ethereal sulphates is 
as 10 is to I, and is found to vary widely in disease. 

Diminution. — The total sulphates are found diminished 
when upon a vegetable diet, during convalescence, in chronic 
renal disease, non-obstructive jaundice, diarrhea, and during 
starvation. A strongly acid gastric fluid (due to lactic and butyric 
acids) and alcoholic excesses may cause a diminished elimina- 
tion of the ethereal sulphates. 

Detection and Approximate Estimation. — Reagents. — i. 
Solution of barium chlorid (i part to 8). 

2. Acetic acid (specific gravity, 1.04). 

Application. — i. Place 10 c.c. of urine in a test-tube. 

2. Acidify with acetic acid. 

3. Add about 3 c.c. (one- third volume) of barium chlorid 
solution — I c.c. at a time, shaking gently after each addition. 

Reaction. — A white, milky precipitate indicates the presence 
of sulphates in normal amounts; but should the liquid assume 
the consistence of cream, sulphates are present in excess. If the 
liquid becomes opalescent, sulphates are diminished. 



1 86 THE URINE. 

Quantitative Estimation of Total Sulphates. — Reagents. — 

1. Hydrochloric acid (specific gravity, 1.12). 

2. Saturated solution of barium chlorid. 

Application. — i. One hundred c.c. of filtered urine are placed 
in a beaker and treated with 8 c.c. of hydrochloric acid (i), and 
heated over a v^ater-bath to boiling. 

2. Twenty c.c. of barium chlorid solution (2) are now added, 
and heat continued until the barium has thoroughly settled as 
barium sulphate, and the supernatant liquid is clear (occupying 
from twenty to forty minutes). 

3. Filter through a Gooch funnel (Fig. 73) that is provided with 
a plug of asbestos ; all having been dried and weighed. 

4. Small quantities of water are to be added to the last cubic 
centimeter, and the final portion is placed 
upon the filter by means of a rubber-tipped 
glass rod. 

Caution. — Never allow the filter to 
become dry during filtration. 

5. Wash the precipitate with boihng 
water until the wash- water is clear and 
remains clear after a drop of dilute sul- 
phuric acid has been added. 

6. Remove all gum-like substances by 
washing with hot alcohol (70 per cent.). 

7. Fill the filter two or more times 
Fig. 73.— Gooch filter or funnel, with ctlier. When a paper filter has been 

employed, it is placed in a porcelain 
crucible of known weight, and ignited. The crucible is nearly 
covered by the lid and the ash heated moderately for a time. It 
is then half covered and heated further until the ash becomes 
w^hite, and after coohng the crucible is placed in a desiccator and 
weighed. The difference between the first and second Aveights 
equals the weight of barium sulphate found in 100 c.c. of urine. 
A portion of sulphate is reduced through combustion in the 
presence of organic matter, so that the weight obtained is too 
low; therefore wash the barium sulphate into a beaker with a small 
quantity of water colored red by a few drops of an alcohohc solu- 
tion of phenolphthalein. This Hquid is titrated with a one-tenth 
normal solution of sulphuric acid until the red color disappears. 
Each cubic centimeter of the one-tenth normal solution corre- 
sponds to 0.004 gi^- of barium sulphate. The figure obtained 
in this manner is added to that acquired by weighing, and the 
amount equals the total barium sulphate derived from 100 c.c. 
of urine. 




SULPHATES. 187 

Quantitative Estimation of the Ethereal (Conjugate) 
Sulphates. — Reagent. — Alkaline solution of barium chloric!. 

Dilute hydrochloric acid. 

Application. — i. Place 100 c.c. of filtered urine in a beaker; 
add 100 c.c. of barium-chlorid solution, and stir thoroughly. 

2. After standing a few minutes filter into a graduate up to 
the loo-c.c. mark. 

3. Acidify strongly with dilute hydrochloric acid and boil on 
a water-bath until the barium sulphates which form settle. 

4. Filter, wash, dry, and weigh precipitate (see above). 
The weight thus gained is multiplied by two and the product 

equals the ethereal sulphates in 100 c.c. of urine, and when this 
is deducted from the amount of total sulphate formed, the difference 
will equal the amount of mineral (preformed) sulphates. 

Estimation of Neutral Sulphur. — The oxidized sulphur, 
mineral and ethereal sulphates are estimated as before described, 
and the difference between the sum of these and total amount of 
sulphur equals the amount of neutral sulphur present. 

Reagejits. — i. Mixture of sodium and potassium carbonate 
(11 to 14). 

2. Potassium permanganate (crystalline). 

3. Concentrated hydrochloric acid. 

4. Saturated solution of barium chlorid. 

Application. — i. One hundred c.c. of urine are treated with 
12 gm. of sodium-potassium-carbonate mixture, and evaporated 
to dryness in a nickel crucible. 

2. Fuse the residue, cool, and extract with hot water. 

3. Filter off the carbonaceous residue. 

4. Treat the filtrate and washings with a few crystals of potas- 
sium permanganate and heat for fifteen minutes, when more 
potassium permanganate is added, and heat continued; should 
the solution become decolorized, the heat is prolonged fifteen 
minutes longer. 

5. Add concentrated hydrochloric acid until a decided acid 
reaction is obtained. 

6. Boil this solution and treat with 20 c.c. of the barium- 
chlorid solution, and proceed further as described under the 
Estimation of Total Sulphates (page 186). 

Loosely Combined Sulphur in the Urine. — This is a factor 
many chemists regard as a pre-eminent feature which distinguishes 
Bence- Jones' albumose from the digestive albumoses, as well as 
as from histon and globin (see Albumosuria, page 217). 

The Author's Method.* — i. Fifteen to 20 c.c. of filtered urine 

* "Amcr. Jour. Med. Sci.," Oct., 1902, p. 567. 



i88 



THE URINE. 



are placed in a test-tube, and to it an equal quantity of a saturated 
solution of sodium chlorid is added, shaking the tube to insure a 
_ mingling of the hquids. 

2. Two or three c.c. of a 30 per cent, solution 
of caustic soda are now added, the shaking con- 
tinuing vigorously. 

3. The upper one-fourth of this column of 
liquid is gradually heated over a flame to the 
boiling-point, when a solution of lead acetate (10 
per cent.) is added drop by drop, the upper 
stratum of liquid being boiled after each addi- 
tional drop. 

4. When the drop of lead solution comes in 
contact with the liquid, a copious, pearly or 
creamy, cloud appears at the surface, becoming 
less dense as the boihng-point is neared; and 
when ebullition is prolonged for from one-half 
to one minute, the upper portion of the liquid 
shows slight browning, which deepens to a dull 
black color, as shown by the accompanying illus- 
tration (Fig. 74). 

Below this point for some distance is seen 
a variable degree of browning (2). Standing 
intensifies the reaction, and if this be pro- 
longed for several hours, the black precipitate 
falls through the clear stratum of liquid (3), 
collecting in the bottom of the tube as a coarsely 
granular pigment. Personally, this method has 
been employed in the study of four cases of 
Bence- Jones' albumosuria — dilution, i part in 10, 
and often a much higher dilution gave positive 
results. 

Another method worthy of mention is to 
place a quantity of urine in a beaker and 
heat on a water-bath to from 54° to 60° C, 
then cool and filter. The precipitate collected 
is dissolved by washing with a solution of soda 
(specific gravity, 1.16). The precipitate is 
now heated to the boihng-point, when a 10 
per cent, solution of lead acetate is added drop 
by drop, and the boiling continued. The 
creamy precipitate which first appears soon 
shows evidence of browning and changes later 
to dull black. 




Fig. 74. — Author's 
reaction for Bence- 
Jones' alburaose. 



CENTRIFUGAL ANALYSIS. 



189 



CENTRIFUGAL ANALYSIS. 

This method of determining the quantity of inorganic sub- 
stances present in the urine, while only approximately estimating 
the chlorids, phosphates, and sulphates, gives results which ap- 
proach accuracy as nearly as is required in most clinical work. 
Its daily use in the author's laboratories has proved it to be of effi- 
cient service and worthy of special mention, since it is possible 
through it to estimate in twenty minutes the inorganic constituents 
of a given urine. 

The equipment necessary is a centrifuge (Fig. 75) with a stand- 





FJg- 75- — Water-motor centrifuge. 



Fig-. 76. — Purdy's tubes 
for the centrifuge : a, Per- 
centage tube ; b, sediment 
tube. 



ard radius of arm and tube, capable of a speed of 1200 revolutions 
per minute, and Purdy's graduated percentage tubes (Fig. 76). 

Estimation of Chlorids. — Fill the tube with fikered urine 
to the lo-c.c. mark, and add i c.c. of strong nitric acid and 4 c.c. 
of the standard silver-nitrate solution (AgNg, 5j, distilled water, 
Sj). Place the thumb over the mouth of the tube and invert 
it three or four times to effect a complete minghng of the urine 



I go 



THE URINE. 



and reagents. Allow it to stand for three minutes and then 
place in the centrifuge at the speed indicated for three minutes, 
when the amount of precipitate is read. By consulting the 
accompanying table (which was devised by the late Dr. Purdy) 
the amount of AgCl present can be determined. 

TABLE FOR THE ESTIMATION OF CHLORIDS AFTER CEN- 
TRIFUGATION. 



Showing the hulk-percentage oj silver chlorid {AgCl) and the corresponding 
gravimetric percentages and grains per flicidounce oj sodium chlorid 
(NaCl) and chlorin {CI). — {Purdy.) 



u 

< 






















1 


u 


d 


c 
< 

H 
Z . 


u 





u 


u 


IS 


o 
< 





I 







< 


c 


a 

< 







z 


a 




pi 


a< 


Z 


ai 


h 
Z 


a 


MO 


u 


c 


a 
u 


o^ 


l^ 




£ 




a 


iJ 


o: 




K 






pJ 




Ci 




D 


td 


d 




ii 


■z 




:i' 


a 


d 


Ui 


Ph 


G 


^ 


c 


^ 


1.04 





t. 





\ 


0.03 


0.15 


0.02 


O.I 


8 


4.98 


0.63 


3.02 


h 


0.07 


0.31 


0.04 


0.19 


8i 


I.I 


5-29 


0.67 


3.2Z 


1 


O.I 


0.47 


0.06 


0.28 


9 


1. 17 


5-6 


0.71 


3-4 


I 


0.13 


0.62 


0.08 


0.38 


9i 


1.23 


5-91 


0-75 


3-6 


li 


0.16 


0.78 


0.1 


0.48 


10 


1-3 


6.22 


0.79 


3-79 


I§ 


o.ig 


0-93 


0.12 


0-57 


IO§ 


1.36 


6-53 


0.83 


3-97 


if 


0.23 


1.09 


0.14 


0.66 


II 


1-43 


6.84 


0.87 


4.16 


2 


0.26 


1.24 


0.16 


0.76 


iii 


1.49 


7.2 


0.91 


4-35 


2i 


0.29 


1.41 


0.18 


0.85 


12 


I.S6 


7.46 


0-95 


4-54 


2* 


0.32 


1.56 


0.2 


0.96 


I2i 


1.62 


7.78 


0.99 


4-73 


2| 


0.36 


1. 71 


0.22 


1.04 


13 


1.69 


8.09 


1.02 


4.92 


3 


0-39 


1.87 


0.24 


1-13 


i3i 


1-75 


8.4 


1.06 


5-II 


3i 


0.42 


2.02 


0.26 


1.23 


14 


1.82 


8.71 


I.I 


5-29 


3i 


0.45 


2.18 


0.28 


1.32 


144 


1.88 


9.02 


1. 14 


5-49 


3l 


0.49 


2-35 


0-3 


1.42 


15 


1.94 


9-33 


1. 18 


5-67 


4 


0.52 


2.49 


0.32 


1-51 


154 


2.01 


9-65 


1.22 


5.86 


4i 


0.55 


2.64 


0.34 


1. 61 


16 


2.07 


9-94 


1.26 


6.06 


4i 


0.58 


2.8 


0-35 


1-7 


16J 


2.14 


10.27 


1-3 


6.24 


4l 


0.62 


2.96 


0-37 


1.8 


17 


2.2 


10.51 


1-34 


6.43 


5 


0.65 


3-II 


0-39 


1.89 


i7i 


2.27 


10.87 


1.38 


6.62 


Sh 


0.71 


3-42 


0.43 


2.09 


18 


2-?>3 


II. 2 


1.42 


6.81 


6 


0.78 


3-73 


0.47 


2.27 


i8| 


2.4 


11.51 


1.46 


7.0 


6\ 


0.84 


4-05 


0.51 


2.46 


19 


2.46 


11.82 


1-5 


7.19 


7 


0.91 


4-35 


0-55 


2.62 


194 


2-53 


12.13 


1.54 


7.38 


7i 


0.97 


4.67 


0-59 1 


2.84 


20 


2-59 


12.44 


1.58 , 


576 



Bulk-percentage to be read on the side of the tube. 

Estimation of Phosphates. — Proceed as in the estimation 
of chlorids, except to add 2 c.c. of 50 per cent, acetic acid and 
3 c.c. of a 5 per cent, uranium-nitrate solution. The bulk-percent- 
age of uranyl phosphate (H[U.02]POJ is read and calculated 
in accord with the table for phosphates. 



CENTRIFUGAL ANALYSIS. 



191 



TABLE FOR THE ESTIMATION OF PHOSPHATES AFTER CEN- 
TRIFUGATION. 



Showifig hulk-percentages of uranyl phosphate {H[UO^PO^ and 
sponding gravimetric percentages and grains per ounce of 
phosphoric acid (P20^). — (Purdy.) 



the cor re- 



Bulk-per- 
centage OF 
H(U0o)P04. 


Percentage 
P2O5. 


Gr. Per Oz. 

P-205. 


Bulk-per- 
centage OF 
H(U0.2)P04. 


Percentage 
P.Oi. 


Gr. Per Oz. 
P-.Oo. 


i 


0.02 


0.1 


II 


0.14 


0.67 


I 


0.04 


0.19 


12 


0.15 


0.72 


li 


0.45 


0.22 


13 


0.16 


0.77 


2 


0.0^ 


0.24 


14 


0.17 


0.82 


2h 


0.055 


0.26 


15 


0.18 


0.86 


3 


0.06 


0.29 


16 


0.19 


0.91 


3^ 


0.065 


0.31 


17 


0.2 


0.96 


4 


0.07 


0.34 


18 


0.21 


1.06 


4h 


0.075 


0.36 


19 


0.22 


1.06 


5 


0.08 


0.38 


20 


0.23 


I-I5 


6 


0.09 


0-43 


21 


0.24 


I-I5 


7 


0.1 


0.48 


22 


0.25 


1.25 


8 


O.II 


0-53 


23 


0.26 


1.25 


9 


0.12 


0.58 


24 


0.27 


1-35 


10 


0.13 


0.62 


25 


0.28 


0.35 



Bulk-percentage to be read from graduation on the side of the tube. 

Estimation of Sulphates. — Proceed as in estimating chlorids, 
except to add 5 ex. of barium-chlorid mixture (barium chlorid 
4 parts, strong hydrochloric acid i part, distilled water 16 parts). 
The precipitate of barium sulphate (BaSOJ is estimated by the 
table for sulphates. 



TABLE FOR THE ESTIMATION OF SULPHATES AFTER CEN- 
TRIFUGATION. 

Showing the hiilk-percentages of barium sulphate {BaSO^ and the corresponding 

gravimetric percentages and grains per fliiidounce of sulphuric 

acid {SO^).—{Piirdy.) 



Bulk-per- 
centage OF 
BaSOi. 


Percentage 
SO3. 


Gr. Per Oz. 
SO3. 


Bulk-per- 
centage OF 
BaS04. 


Percentage 
SO3. 


Gr. Per Oz. 

SO3. 


\ 


0.04 


0.19 


2i 


0-55 


2.64 


1 

t 


0.07 
0.1 


0.34 
0.48 


2i 
2I 


0.61 
0.67 


2-93 
3.22 


h 


0.13 


0.62 


3 


0.73 


3-5 


1 


0.16 
0.19 


0.77 
0.91 


3i 
2>h 


0.79 
0.85 


3-79 
4.08 


1 


0.22 


1.06 


3l 


0.91 


4-37 


I 


0.25 


I.I 


4 


0.97 


4.66 


I^ 


0.31 


1.49 
1.78 


i 


1.03 
1.09 


4.94 
5-23 


if 


043 


2.06 


4f 


1-15 


5-52 


2 


0.49 


2-35 


5 


1. 21 


5.81 



Bulk-percentage to be read from graduation on the side of the tube. 



192 THE URINE. 

Should the bulk-percentage exceed 15 per cent., the urine should 
be diluted. 

For description of Wetherill's method of torfugation see p. 528. 



UREA. 

Urea is the most abundant of all the smgle constituents of 
normal urine, 20 to 40 gm. (300 to 600 gr.) being excreted by 
a healthy man of average weight during the twenty-four hours. 
The greater portion of nitrogen taken with the food is excreted 
through the urine as urea; therefore retrograde tissue metamor- 
phosis and the unassimilated principles of nitrogenous foods 
directly influence the elimination of urea. 

Urea, CO(NH2)2, when crystalline, appears as colorless, quadri- 
lateral or hexagonal, silky prisms, with rather oblique ends; 

or, when rapidly crystallized, 
as dehcate needles. These 
crystals are permanent in air, 
but soluble in water. When 
treated with nitric acid, nitrate 
of urea (CON^H^HNOg) is 
formed as hexagonal, octa- 
hedral, or lozenge-shaped 




crystals, not freely soluble in 
water. 

At 100° C. urea gives evi- 
dence of decomposition and 
melts at 130° to 132° C. Dur- 
ing decomposition biuret is 
formed (see Biuret Reaction, 

Fig. 77. — Crystals of nitrate of urea (upper half) ^n 

and oxalate of urea (lower half) (Ogden). P^&^ ^ I / j • 

Approximately 85 per cent, 
of the nitrogen eliminated in the urine is found in the form of 
urea; the remaining nitrogen consisting of uric acid, kreatinin, 
hippuric acid, and xanthin bases. It is impossible, however, to 
estimate the destructive tissue-changes taking place in the body 
from the quantity of urea eliminated. 

The mean amount for healthy men between twenty and forty 
years is 33.18 gm. (512.4 gr.), and is 0.015 to 0.035 gm. per 
hour for each kilogram (approximately 2 pounds) of body- weight. 
Women excrete less urea than men, while children excrete propor- 
tionately more than either men or women. 

Increase. — An increased eHmination of urea is observed in 
the acute febrile diseases and is due to increased tissue-destruction; 
— 50 gm. are frequently excreted in twenty-four hours both during 



UREA. 193 

the fastigium as well as at the time of, and following, the crisis. 
Such non-febrile conditions as diabetes melhtus, dyspnea, perni- 
cious anemia, scurvy, leukemia, paralysis agitans, minor chorea, 
epilepsy, gastro-intestinal disorders, functional albuminuria; as 
well as the following drugs — caffein, ammonium chlorid, potassium 
chlorid, morphin, codein, and carbonate of lithia — cause an in- 
creased excretion of urea. An increase also follows phosphorus- 
poisoning and the apphcation of electricity. 

Decrease. — A decreased elimination of urea is encountered 
in acute yellow atrophy. It may even be absent and such other 
nitrogenous bodies as leucin and tyrosin found in its stead. 
Hepatic cirrhosis and carcinoma, Weil's disease (a pecuhar form 
of infectious jaundice), chronic plumbism, chronic rheumatism, 
chronic nephritis, osteomalacia, general paresis, melanchoha, 
hysteric outbreaks, catalepsy, Addison's disease, and chronic 
alcoholism display a decreased elimination, possibly of a nervous 
character. It has been noted in leprosy and in impetigo. In- 
hibited hepatic circulation, or excretion and destruction of liver 
tissue with gastro-intestinal derangements, play important roles 
in diminishing the elimination of urea. 

Ratio. — The proportionate relation existing between the 
ehmination of urea, phosphates, and chlorids — the latter equaHng 
about one-half that of the urea during health — will often be found 
of interest. 

Quantitative Estimation of Urea. — A number of methods 
have been devised for the estimation of urea in the urine, which 
with but few exceptions depend upon its decomposition and the 
estimation of the nitrogen evolved during this process, or by the 
difference in density of the urine before decomposition and after 
it is completed. 

Hypobromite Method. — This is by far the most practical 
method for clinical purposes, despite the moderate degree of error 
to which it is hable, as it is based upon the decomposition of urea 
into carbon dioxid and nitrogen when in the presence of sodium 
hypobromite. The excess of sodium-hydrate solution absorbs 
the CO2, leaving only the nitrogen to be estimated. 

Reagents. — i. NaOH 100 parts, and H2O 250 parts. 

2. Bromin i part, KBr i part, Hfi 8 parts. Mix these 
solutions in proportions of one part of No. 2 to four parts of No. i. 

The hypobromite solution (dissolve 100 gm. of caustic soda in 
250 c.c. of water and permit to stand until it is cool, when 25 
c.c. of bromin are added) if placed in amber or green glass- 
stoppered bottles and kept in a cool place, will keep for a fort- 
13 



194 



THE URINE. 



night. Many writers prefer a much weaker solution; while 
others again have two solutions, and mix them together when 
needed. It is with this latter method that I have obtained the 
most satisfactory results. 

A number of forms of apparatus have been devised, but the 
one which appears to be most convenient is that lately recom- 
mended by Doremus (Figs. 78, 79). 

Procedure. — i. A small amount of urine is placed in tube (c) 




/^ 




Fig. 78. — Doremus ureometer. 



Fig. 79. — Hinds' modification of the Dore- 
mus ureometer. 



— Stop-cock {h) closed — and the stop-cock is opened for a moment 
and then closed in order to fill its lumen. 

2. Notice that both tubes are now free from urine, and fill 
tube (a) with the hypobromite solution. 

3. Next place the urine in tube (c). 

4. The stop-cock is now^ turned slightly and the urine is 
allowed to mingle slowly with the hypobromite solution until 
one-half or one c.c. has passed from {c) to {a). The nitrogen 
generated is collected at the top of {a). The degrees graduated 
indicate the amount of urea (in grams or grains) in the quantity 
of urine employed. 

Caution. — Should the urine be concentrated, a dilution of 
one part of urine in 4 or even in 10 parts of water will give more 
constant readings, which are to be multiplied by the amount of 



UREA. 195 

dilution used. Again, thermic fluctuations are known to influence 
the reading slightly, but for chnical purposes this is not worthy 
of consideration. 

Estimation of Total Nitrogen. — The method suggested by 
Kjeldahl will serve as one convenient for this purpose; the first 
step being to decompose the organic matter by means of sulphuric 
acid, when all nitrogen not in combination with oxygen is con- 
verted into ammonia. An excess of sodium hydrate is now added 
and distilled, received into a known quantity of titrated acid, and 
the excess again titrated with sodium hydrate; thus ascertaining 
the amount of ammonia requisite. Since 17 gm. of ammonia 
correspond to 14 gm. of nitrogen, the quantity of nitrogen is 
readily ascertained. 

Reagents. — i. Gunning's mixture — 15 c.c. concentrated sul- 
phuric acid; 10 gm. potassium sulphate; 0.5 gm. copper sulphate. 

2. Solution sodium hydrate (270 gm. to 1000 c.c, specific 
gravity, 1.243). 

3. Pulverized talcum or granulated zinc. 

4. A one-fourth normal solution sulphuric acid. 

5. A one-fourth normal solution sodium hydrate. 
Application. — i. Ten c.c. of urine are placed in a flask and 

treated with reagent (i). The flask is placed at an angle of 45 
degrees and heated just to the boiHng-point, until the solution 
is clear. 

2. Cool and transfer the contents of the flask to a retort with 
the aid of water, and treat with a shght excess of sodium hydrate 
solution (5) (40 c.c. of which will equal 5 c.c. of sulphuric acid). 

3. Add a small amount of talcum or granulated zinc (3), con- 
nect retort with the condenser, and begin distillation, continuing 
until two-thirds of the solution has passed over. The nitrogen 
bulb into which the distillate is received should contain a definite 
quantity of a one-fourth normal solution of sulphuric acid (4), 
of which 25 to 35 c.c. are usually required. Disconnect the con- 
denser whenever the distillation is completed, and wash it with 
distilled water, adding the washing to the distillate. 

4. Add a few drops of tincture of cochineal or phenolphthalein. 

5. Titrate the excess of sulphuric acid with the one-fourth 
normal solution of sodium hydrate (5), and the quantity found to 
be present is deducted from the 30 c.c. employed. Continue the 
titration until the yellow is replaced by a rose color. The difl'er- 
ence multiphed by 0.0035 equals the amount of nitrogen present 
in the 10 c.c. of urine; but if, instead, the figure representing tliis 
difference be multiphed by 20, it is equivalent to the amount of 
urea present in the 10 c.c. of urine. 



196 THE URINE. 

URIC ACID. 

Uric acid results from the decomposition of a certain variety 
of albuminous substance — nucleins. The nuclear nucleins (con- 
taining a nucleinic acid radicle) appear to constitute the mother 
substance of uric acid. Paranucleins are known to be deficient 
in this particular, and they in no way influence the ehmination of 
uric acid. 

The daily ehmination for normal man is found to be between 
0.2 and 0.5 gm. Kossel has demonstrated forms of nucleinic acid 
which are known as the xanthin, alloxur, or purin bases, and, 
according to Fischer, are probably derived from purin. Mono- 
methyl- xanthin or heteroxanthin, dimethyl- xanthin or para- 
xanthin, trimethyl- xanthin, as well as theophylHn and theobromin 
are also closely ahied to this group. 

Uric acid of the urine may be found to occur as a compound 
in which one molecule of sodium is combined with tw^o molecules 
of uric acid. The conditions affecting its solubihty are the quan- 
tity of water, presence of inorganic salts, and the reaction of the 
urine. Uric acid is precipitated from urines containing an excess 
of disodic phosphate. Such basic substances as sodium, am- 
monium, and potassium are known to occur with uric acid, and 
when these salts are decomposed by strong acids, uric acid is 
set free. Uric acid in its purity occurs as colorless rhombic 
plates, but that which precipitates from the urine is oftenest of a 
reddish-brown hue (see Microscopy, page 264). 

Increase. — After the ingestion of such foods as Hver, kidney, 
thymus gland, and brain, — rich in either the purin bases or in 
nuclear nucleins, — an increased ehmination occurs. It also takes 
place after excessive cell destruction of the body tissues, especially 
the leukocytes, five hours after a full meal ; during and immediately 
after a paroxysm of gout; in acute articular rheumatism with 
high temperature; and in leukemia the ehmination is increased. 
In the latter condition it has been known to reach 5 gm. per diem. 

Decrease. — A decreased ehmination may be noticed as the 
result of a purely vegetable diet; preceding an attack of gout; 
during the course of diabetes, chronic plumbism, chronic inter- 
stitial nephritis, pseudo-hypertrophic paralysis, progressive mus- 
cular atrophy, and in chlorosis. In the secondary and pernicious 
types of anemia decreased ehmination is also a prominent feature. 

Tests for Uric Acid. — Murexid Test.— i. Place a few crys- 
tals of uric acid on a porcelain dish, add 5 to 10 drops of con- 
centrated nitric acid, and heat sufficiently to evaporate the acid. 
A yellowish-red color remains upon the porcelain. 



URIC ACID. 197 

2. Cool, and add a drop of ammonia, when a purplish- red 
color develops (murexid). 

3. A drop of sodium hydrate causes this to change to a reddish- 
blue color which disappears on heating. 

Copper Test. — i. Dissolve crystals of uric acid in a solution 
of sodium hydrate. 

2. Treat the mixture with Fehhng's solution and heat, when 
a white precipitate will develop (white urate of copper), but should 
sufficient Cu sulphate be present, a reddish precipitate appears 
(cuprous oxid). 

Carbonate-of-silver Test. — i. Dissolve crystals of uric acid 
in a solution of sodium or potassium carbonate. 

2. Place a few drops on a paper, and to it add a drop or 
two of a solution of nitrate of silver, when a distinct gray stain 
occurs. Urates also cause this reaction. 

Quantitative Estimation of Uric Acid. — Reagents. — Dis- 
solve 1.58 gm. of potassium permanganate in one liter of water 
(i c.c. of this solution is decolorized by 0.00375 gm. of uric acid). 
Place 100 c.c. of clear filtered urine into a beaker, and to it add 35 
gm. of pure ammonium chlorid; stir well, and to the mixture add 
ammonia and water to give it an alkaHne reaction. Agitate the 
fluid by stirring for five minutes, then allow it to stand for five 
minutes, by which time a precipitate will have settled near the 
bottom of the beaker. This precipitate is composed of earthy 
phosphates together with the whole of the uric acid as hydrogen 
ammonium urates. Filter and wash with a saturated solution 
of ammonium chlorid the precipitate which collects upon the 
filter. Remove the funnel and wash the precipitate into a beaker 
by means of a jet of water from the wash-bottle. The funnel is 
returned to its support, and underneath it is placed the beaker 
into which the precipitate has been washed. Hot w^ater contain- 
ing a trifle of sodium carbonate is now poured through the filter. 
Repeat this process three times, heat the beaker and its contents, 
and then add 10 c.c. of concentrated sulphuric acid. A decidedly 
acid reaction is produced. Immediately titrate with a standard 
solution of potassium permanganate, and the percentage of uric 
acid in the urine is estimated from the number of cubic centi- 
meters of permanganate solution employed. 

Reaction. — A weak solution of potassium permanganate dis- 
plays a decided rose color which it loses instantly when allowed 
to flow slowly into the hot solution of uric acid in dilute sulphuric 
acid, shaking after each addition of the permanganate solution. 
This disappearance of the rose coloring of the permanganate 
solution is caused by the uric acid, which rapidly decomposes the 



198 THE URINE. 

potassium permanganate. Whenever a single drop in excess of 
the potassium permanganate is added, its rose color persists and 
the end point oj the titration is thus placarded. Titration must 
be carried out at a temperature between 60° and 80° C. 

Method of Computation. — The percentage of uric acid present 
in the given specimen of urine is determined in the following 
manner: 

0.00375 X No. c.c. of permanganate solution employed. In 
every 100 c.c. of urine o.ooi gm. of uric acid escapes precipita- 
tion, therefore it requires this addition to the final product. The 
results obtained by this method, while sufficiently rehable for 
general clinical work, should not be compared with those obtained 
by the more comphcated methods. 

Ludwig-Salkowski's Method. — This method is based upon 
the principle that a solution of uric acid in sodium carbonate 
treated with a solution of nitrate of silver — an excess of ammonia 
having previously been added to the mixture — induces a flaky 
gelatinous precipitate composed of uric acid, silver, and sodium; 
this precipitate being only feebly, if at all, soluble. The silver 
may ' be removed, leaving compounds of uric acid and sodium 
capable of decomposition by the addition of hydrochloric acid. 

Precautions. — i. Concentrated urines should be diluted one- 
half. 

2. The specific gravity should be nearly 1.020, and urines of 
a lower specific gravity should be evaporated to approximate this 
density. 

3. When there is a distinct deposit of uric acid at the bottom 
of the urine to be examined, this too should be collected and 
estimated. 

4. Albumins should be removed from the urine. 

5. In case the urine contains sugar, from 500 to 1000 c.c. are 
treated with a neutral solution of acetate of lead; this is filtered, 
and the filtrate is then precipitated with mercuric acetate. This 
precipitate consists mostly of mercuric urates, and after having 
stood for twenty-four hours, should be separated by filtration. 
Wash and suspend in water. Remove the mercury by means 
of sulphureted hydrogen, filter off the sulphid of mercury, and 
preserve the filtrate. Thoroughly boil the precipitate with water, 
again filter, and the washing obtained is added to the filtrate pre- 
viously preserved. Evaporate the total quantity of fluid to a 
rather small volume; acidify with hydrochloric acid, when the 
uric acid separates out and may be treated by one of the methods 
previously named. 



URIC ACID. 199 

6. It is essential that rapidity be exercised while conducting 
the various steps in Ludwig-Salkowski's method. 

Method of Application. — Reagents. — i. Ammoniacal mag- 
nesium mixture. Dissolve 100 gm. of crystalhzed magnesium 
chlorid in a suihcient quantity of water, and to it add (cold) 
a saturated solution of magnesium chlorid in excess, and sufficient 
strong ammonium to lend a decided odor to the mixture. Where 
the mixture remains cloudy add more ammonium-chlorid solution. 
Dilute to a hter and place in a glass-stoppered bottle. 

2. Dissolve 26 gm. nitrate of silver in distilled water, and then 
add ammonia sufficient to dissolve the brown precipitate. Dilute 
to a Hter and place in a colored, glass-stoppered bottle. 

Place in a vessel 250 c.c. of filtered urine and treat with 50 
c.c. of ammoniacal magnesium mixture to remove the phosphates. 
Filter immediately, thereby preventing the formation of a small 
amount of magnesium urate. Place 250 c.c. of the filtrate, which 
corresponds to 200 c.c. of the urine, in a vessel and treat with a 
solution of nitrate of silver (3 per cent.). Should the precipitated 
silver chlorid, which forms soon after the addition of the silver, 
disappear on stirring, add a few drops of ammonium hydrate. A 
flaky precipitate now separates and is allowed to settle. Acidify 
a few cubic centimeters of the supernatant fluid with nitric acid 
to determine whether or not enough of the silver-nitrate solution has 
been added, and in the event of a distinct clouding, suggestive of 
silver chlorid, sufficient of the silver solution has been added. 
Should this clouding not appear, the mixture needs to be rendered 
-alkahne with ammonium, returned in the beaker, and again treated 
with the silver solution. Filter rapidly through a rather loose 
paper, all precipitates being removed from the beaker by means of a 
glass rod. Wash the precipitate until the specimen of the wash- 
ing is not rendered turbid by nitric acid, and until only a sHght 
turbidity follows the addition of a drop of silver solution. The 
precipitate and the filter are placed in a wide-mouthed flask which 
contains about 200 c.c. of distilled water. Agitate vigorously. 
Pass sulphureted hydrogen through the mixture, bring to the 
"boihng-point, and render distinctly acid by adding a few drops of 
hydrochloric acid; at which time the sulphid of silver and the 
paper are rapidly separated by filtering. Should this separation 
be effected slowly, there is liable to be an admixture of silver to 
the uric acid. Wash the contents of the filter several times with 
hot water, and quickly evaporate both the filtrate and the wash- 
ings to but a few cubic centimeters. Add a few drops of hydro- 
chloric acid and allow to stand in a cool place for twenty-four 
hours. When the mixture contains silver there is a cloud following: 



200 



THE URINE. 



the addition of the hydrochloric acid. The dried uric acid needs 
to be washed with carbon disulphid. Collect the uric acid that 
has separated from the solution on a dried and weighed filter. 
Wash with water, then with 90 per cent, alcohol, and finally with 
absolute alcohol and ether. The water employed for washing 
should be collected separately, and for every 20 c.c. ,used 0.0048 
gm. should be added to the weight of the uric acid obtained. 



XANTHIN BASES, 

Collectively the substances comprising the xanthin bases and 
uric acid are referred to as the alloxur bases and the purin bases. 
The xanthin bases of the urine are xanthin, hypoxanthin, hetero- 
xanthin, paraxanthin, adenin, and guanin; and unlike uric acid,. 

xanthin bases are to be found 
in both animal and vegetable 
tissues. Under normal con- 
ditions the urine will be found 
to contain a very small per- 
centage of xanthin, amount- 
ing in bulk to about 10 per 
cent, of the uric acid. As a 
rule, it is increased in amount 
when the uric acid shows a 
decided increase. At times, 
however, there is an increase 
in the uric acid together with 
a diminution in the xanthin 
bases; and less frequently the 

Fig. 8o.-Xanthin crystals (after the drawings rCVCrSC COuditioU is met. It 
of Horbaczewski, as represented in Neubauer and 

vogei). is to be remembered that uric 

acid is an oxidation product 
of the xanthin bases, and that its origin is the same, which serves 
to explain their varying proportionate relations. Our present 
knowledge of the xanthin bases and their relation to pathologic 
states is of but limited clinical value. The normal quantity is 
said to fluctuate between 0.0286 and 0.0561 gm. per diem. Para- 
xanthin and heteroxanthin occur but sparingly in the urine. 

Clinical Significance. — The xanthin bases are increased in 
croupous pneumonia, leukemia, nephritis, and after a meal con- 
taining an abundance of nucleins. 

Tests. — (i) Lift a small portion of the urinary sediment into a 
pipet and transfer it to a porcelain dish; (2) add a few drops of nitric 
acid and evaporate to dryness. Should xanthin be present, the 




HIPPURIC ACID. 201 

residue is yellow, but upon the addition of a few drops of sodium- 
hydrate solution and the appHcation of heat, a red color develops. 
This reaction is common to the xanthin bases. 

Quantitative Estimation. — i. Salkowski^s method consists 
in precipitating 600 c.c. of the filtered urine with 200 c.c. of mag- 
nesium mixture (see Ludwig-SalkowskV s ?nelhod, page 198), after 
which add a solution of nitrate of silver (3 per cent.) to 700 c.c. 
of the filtrate in a proportion of 6 c.c. per hundred, observing all 
precautions set forth in Ludwig-Salkowski's method for uric 
acid. 2. Allow the mixture to stand for an hour, filter, and wash 
the precipitate in water until all the free silver has been removed. 
3. Perforate the filter and wash the precipitate into a flask with 600 
to 800 c.c. of water that has been acidified with hydrochloric acid, 
and decompose with sulphureted hydrogen. 4. Heat over a water- 
bath to remove any excess of sulphureted hydrogen; filter to 
separate the sulphid of silver and evaporate the filtrate to dryness. 

5. Treat the residue with 30 c.c. of sulphuric acid (i-ioo); 
boil the solution, and then allow it to stand for twelve hours. 

6. The uric acid will be found to have separated from the 
liquid, which should be filtered, washed with a small amount of 
dilute sulphuric acid, and later with alcohol and ether, and weighed. 
Add 0.0005 gm. to the result for every 10 c.c. of the acid filtrate 
employed — allowing for the trace of uric acid thus lost. 

7. After the uric acid has been removed by filtration, the filtrate 
is treated a second time with ammonium and silver solution to 
precipitate the xanthin bases. 8. Collect this precipitate on a filter, 
wash with water, dry, and incinerate. 9. Dissolve the ash in nitric 
acid and the silver is estimated by titration with a solution of 
potassium sulphocyanid, using ammonioferric alum (saturated 
solution at ordinary temperature) as an indicator. The solution 
of potassium sulphocyanid described in the estimation of the 
urinary chlorids (page 180) may be employed, and this solution 
is of such strength that i c.c. corresponds to 0.00734 gm. of 
silver. One atom of silver when in combination with silver 
compounds of xanthin, guanin, etc., represents 0.277 g^- of 
nitrogen or 0.7381 gm. of alloxur bases. One c.c. of the potas- 
sium sulphocyanid solution represents 0.002 gm. of nitrogen and 
likewise 0.00542 gm. of alloxur bases. 

HIPPURIC ACID. 

Under normal conditions from o.i to i gm. of hippuric acid 
is excreted through the urine during every twenty-four hours. 
This is probably derived largely from albuminous material. The 



202 THE URIXE. 

elimination continues during the administration of albuminous 
materials as well as during starvation. It usually occurs in com- 
bination with potassium, magnesium, sodium, and calcium; and 
is readily soluble in solutions of the alkahne hydrates and carbon- 
ates, alcohol, and ether. Its salts thus formed are decomposed 
bv strong acids, in which instance hippuric acid separates out and 
may be collected and Aveighed. 

Quantitative Estimation. — Simon's Method. — i. Evaporate 
over a water-bath 500 c.c. of fresh urine to a syrupy consistence, 
keeping the urine neutral in reaction by the addition of sodium 
carbonate during the entire process of evaporation. 2. Extract 
the residue with cold alcohol, 90 to 95 per cent., employing a 
quantity about half that of the urine. 3. Stand the mixture aside 
for twenty-four hours. 4. The alcohohc filtrate will be found to 
contain the salts of hippuric acid, and these are hberated from 
the alcohol by distillation. 5. Acidify the remaining solution 

with acetic acid, and extract 
with five times its own volume 
of alcohohc ether (alcohol i 
part; ether 9 parts). 6. From 
the combined extracts the 
ether is distilled oft' and the 
remaining solution evaporated 
over a water-bath. 7. Boil the 
residue with water, allow it to 

Fig. Si.-Hippuric-acid crystals (Ogden I. ^Ool, and paSS tlirOUgh a Wcll- 

moistened filter. Hippuric 
acid is soluble in boiUng water, and is in this way separated 
from other constituents soluble in alcohol and ether. 8. Render 
the filtrate alkahne with milk of hme, removing all excess of calcium 
by passing carbon dioxid through the mixture, which is later boiled 
and filtered. 9. Shake with ether to remove all impurities, and any 
calcium salts remaining in solution are decomposed by acid, and 
the solution extracted with ether. 10. Evaporate this remaining 
solution to but a few cubic centimeters, and upon standing 
hippuric acid will separate. 11. Dry the crystals upon plaster- 
of-Paris plates, shake with benzol and petroleum-ether for the 
purpose of removing any benzoic acid that may be present, and 
weigh. These crystals of hippuric acid may be recognized under 
the microscope and also by their solubility, etc. 




OXALIC ACID. 203 



OXALIC ACID. 

The oxalic acid in the normal urine is probably derived from 
two sources. One of these is a vegetable diet, while the other 
doubtless exists in the body, though its manner of action is not 
thoroughly understood. This latter variety may be derived from 
the uric acid through oxidation, since oxaluric acid is capable of 
being produced from uric acid, and oxaluric acid is also readily 
decomposed into oxahc acid and urea. Again, oxalic acid may 
result from the imperfect oxidation of carbohydrates. 

Excess. — The excretion of oxahc acid through the urine 
becomes of special pathologic importance since many vegetables 
are capable of causing an excessive ehmination. Among such 
vegetables are spinach, carrots, tomatoes, string-beans, celery, 
and asparagus; and also grapes and apples. Gastro-intestinal 
derangements are hable to cause an increased excretion of oxahc 
acid, which is doubtless the result of incomplete digestion and 
oxidation of carbohydrates. Nervous oxaluria may result in a 
similar manner. 

Transitory albuminuria has been found to be associated with 
oxaluria (Senator), and the late J. M. DaCosta has outhned not 
unlike conditions. In connection with diabetes there are to be 
seen pecuhar relations between the uric acid, carbohydrates, phos- 
phates, and oxalic acid excreted. 

Oxalic-acid Diathesis. — In this condition there is a decidedly 
increased production of oxahc acid accompanied with a tem- 
porary retention which of necessity must later be followed by an 
increased ehmination. This condition does not appear to be 
materially influenced by diet, and may result from abnormal 
metabohc processes within the body tissues. It has been sug- 
gested that this pecuhar production of oxahc acid is not unhke 
that interested in the production of diabetes melhtus, and while 
it is impossible at present to point out clearly the relation existing 
between these two conditions, it is doubtless one deserving of 
further physiologic research. 

The quantity of oxahc acid normally excreted during twenty- 
four hours varies from that of a mere trace to 20 mgm. (0.31 gr.). 
Oxahc acid is readily detected in the urine by its characteristic 
crystals (Fig. 95), though it is impossible to determine with any 
degree of certainty the amount of oxahc acid excreted from the 
number of crystals of calcium oxalate present upon microscopic 
examination. 

Again, urines rich in calcium oxalate may display no crystals 
of this substance even after standing for several hours. It is 



204 THE URINE. 

my practice to neutralize cautiously such urines by adding a few 
drops of ammonia, when it is often possible to induce crystal- 
lization of the salt, and should this procedure be ineffectual, the 
following method must be employed : 

Quantitative Estimation of Oxalic Acid. — i. Treat 600 
c.c. of fresh urine with a small quantity of an alcoholic solution 
of thymol — -in this way preventing putrefaction — and then treat 
it with calcium chlorid and ammonia, adding these substances in 
excess. 2. Diacid sodium phosphate, which holds the oxahc acid 
suspended in solution, is in this way removed, and the precipitate 
is treated with just sufficient acetic acid to dissolve it. 3. The cal- 
cium oxalate being insoluble in acetic acid is gradually precipitated, 
when the mixture is allowed to stand for twenty-four hours. 4. The 
calcium oxalate is now separated by means of a filter; washed with 
a small amount of water and dissolved with a few drops of hydro- 
chloric acid. 5. Add sufficient dilute ammonia to the filtrate to 
give the solution a feebly alkahne reaction; allow to stand for 
twenty-four hours, when the calcium oxalate will have separated 
from the solution and may be collected upon a filter the weight 
of whose ash is known. 

Wash with water the contents of the filter, dry, and incinerate 
in a crucible, heating vigorously for at least twenty minutes, thus 
transforming the oxalate into oxid. The ash is weighed and the 
corresponding amount of oxahc acid calculated. By weight, 56 
parts of calcium oxid are equivalent to 128 of calcium oxalate ; 
therefore 56 : 128 : : }' : x — x being equivalent to 2.2857 y in 
which y is indicative of the quantity of calcium oxid recovered 
from a known quantity of urine. The quantity of calcium oxalate 
is represented by x. 



KREATIN AND KREATININ. 

The former of these substances is constantly present in muscle 
tissue, and is in all probabihty the immediate and perhaps con- 
stant antecedent of kreatinin, which forces one to consider at least 
two sources of this body when found in the urine, namely, the 
body muscular tissue and the ingestion of muscle tissue as food. 
Nearly i gm. of kreatinin represents the daily excretion through 
the urine of a healthy adult. Thus far the pathologic variations in 
the excretion of kreatinin have failed to be of chnical value. The 
increased destruction of body tissue which takes place during the 
course of such febrile conditions as pneumonia and typhoid fever 
may be placarded by an increased elimination of kreatinin in the 
urine. Such patients are not upon a meat diet ; yet parallels have 



PROTEIDS IN THE URINE. 



205 



not been drawn between the excretion of urinary kreatinin under 
such conditions and the destructive changes in the body tissues. 
WeyPs Test. — Treat 10 to 20 c.c. of the urine with a few drops 
of a dilute solution of sodium nitroprussid, and then add to the 
mixture, drop by drop, a weak solution of sodium hydrate. Should 
kreatinin be present in appreciable amounts, the urine becomes 
a ruby- red color; this change being more conspicuous at the 
bottom of the liquid. The red color is but temporary and gives 
way in a few minutes to an intense yellow. Through the apphca- 
tion of heat and the addition of a few drops of glacial acetic acid 
in pure solution, the yellow 
color is replaced by a green. 

PROTEIDS IN THE URINE. 

Any one, or in fact all, of 
the proteids of blood plasma 
may appear in the urine, 
namely, serum-albumin, 
serum-globulin, and fibrin- 
ogen. In addition to these 
it is not uncommon to meet 
with compound proteids — 
mucin and nucleo-albumin 
(normal constituents of the 
urine), and with the albu- 
moses, among which Bence- 

Jones' albumose should be given special mention. It is question- 
able whether true peptone occurs in the urine. Rare, indeed, 
it is that during health any of the pathologic proteids escape 
through the urine. 

Mucin. — Mucin is to be found in normal urine, though but 
a trace may be present; and it is the chief constituent of urine 
containing a large quantity of mucus. Mucin is derived from 
the muciparous glands communicating with the urinary tract. 

Increased. — A decided increase is to be observed in connec- 
tion with a catarrhal condition of the urinary tract, when, 
on standing, it collects at the bottom of the urine in the form of a 
rather heavy, creamy, loose, viscid, slimy, tenacious precipitate. 

Detection. — i. Mucin is precipitated from the urine by vege- 
table acids, such a precipitate being insoluble in an excess of the 
acid employed for its precipitation. (Where the urine contains 
a liberal amount of albumin, first remove this body by boiling 
and filtering.) 2. Add to the precipitate three times its volume 




Fig. 82. — Crystals of kreatiniii-zinc chlorid 
(Salkowski). 



206 THE URINE. 

of Strong alcohol, and set aside for several hours. 3. Filter, wash 
the precipitate with alcohol, and then with warm water. 4. The 
filtrate which contains the mucin is now acidified with acetic 
acid, and should a turbidity appear, mucin is present. 

SERUM-ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 

These substances may occur in the urine either singly or to- 
gether, the latter condition being far more common and con- 
stituting what is ordinarily termed "albuminuria." Albuminuria 
may result from disease of the kidneys, or from acute or chronic 
congestion, etc. The use of drugs, including ether and alcohol; the 
use of albuminous foods; high fever (febrile albuminuria), exer- 
tion, cold baths (functional albuminuria), and standing posture 
(orthostatic albuminuria) may be followed by albuminuria. 

Albumin may originate from congestion or ulcerations of the 
bladder, urethra, vagina or uterus. It follows reduced blood pres- 
sure and occurs late in the anemias. Albuminuria may be co- 
existent with oxaluria, phosphaturia or with diabetes. Accidental 
albuminuria results from an admixture of blood or pus. 

Separation of Albumin and Globulin. — (i) Place a few cubic 
centimeters of urine in a beaker, render it slightly alkaline with 
ammonia, filter to remove the phosphates, and then to 100 c.c. 
of the filtrate add its own volume of a saturated neutral solution 
of ammonium sulphate, allowing it to stand for an hour; by this 
time the globuhn and probably a portion of the mucin will have 
separated from the solution. (2) Collect this precipitate on a 
weighed, ash-free, dried filter, and wash with a solution of ammo- 
nium sulphate, 50 per cent, saturation, after which dry and weigh. 
(3) After drying, incinerate, and detect the weight of the ash, the 
difference being equal to the amount of globulin present. 

The total proteids may be estimated by complete saturation of 
the urine with ammonium sulphate, and drying the precipitate in 
the above manner. The difference between the total proteids 
and the globulin is reckoned as albumin. 

Douglas' Method. — The method which I have adopted 
quite generally for the recognition of albumin, and one which 
appears to have received the sanction of foreign authors (though 
not now popular in America), is the contact method for the de- 
tection of serum- albumin. Carstairs Douglas * has carefully 
determined the quantity of albumin necessary in a given urine to 
produce the characteristic ring upon contact with nitric acid. 
He further studied a series of dilutions made from urines, the per- 
centage of albumin contained in such specimens having been 

* "Chemical and Microscopical Aids to Clinical Diagnosis," 1899, p. 70. 



SERUM-ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 207 

previously ascertained, and concludes that 0.0033 per cent, of 
albumin is sufficient to cause the ring to appear in from two to 
three minutes. For example, a urine after dilution ten times 
showed a ring as above outlined. Multiply 0.0033 by 10 = 0.033 
per cent, of albumin, and in a like manner higher dilutions were 
employed with equally satisfactory results. 

In my experience this method has not served so well as the 
estimation of the total quantity of albumin in the urine by the 
Esbach method (page 211); yet for the average daily estimation 
it is probably sufficiently near to accuracy to enable one to deter- 
mine with safety the amount of albumin as being increased or 
decreased in a given instance. I have been able to obtain better 
results by applying the contact method, using nitric acid, in the 
pipet (see Author's Method), 

Precaution. — In employing Douglas' method the urine 
should be diluted with great care by means of a buret, and at 
least one inch of nitric acid should be placed either in the test-tube 
or allowed to enter the tube (author's method), when the diluted 
urine is brought in contact with it and allowed to occupy a space 
above the acid. The time necessary for coagulation to produce 
the ring is also important, three minutes being the limit. The 
albumin ring is rendered conspicuous by holding the glass or pipet 
containing the urine in front of a dark background. Among 
the various reagents suggested by as many writers I have found 
but two that are capable of withstanding the tests necessary to 
render them worthy of special clinical mention; namely, con- 
centrated nitric acid, and the nitromagnesium mixture (Roberts' 
solution), which is composed of: 

Pure concentrated nitric acid 2 parts 

Saturated solution magnesium sulphate 10 " M. 

The apphcation of these substances as originally outhned by 
Heller was to place a few cubic centimeters of the reagent in a 
test-tube and allow the urine to flow slowly from a buret into the 
tube, where it formed a layer above the reagent. 

Author's Method. — After employing Heller's method for 
some years, the following method of apphcation suggested itself 
to me, and its employment has since been attended with most 
satisfactory results.* Albumin causes a white cloud to appear 
in the form of a ring at the zone of contact of the two Hquids 
(reagent and urine), and this test when carefully apphed must be 
regarded as one of great value. 

I. A pipet is filled for a distance of from one inch to one and 

* "N. Y. Med. Jour.," May 24, 1902, p. 885. 



208 



THE URINE. 



one-half inches with urine to be tested. Then this pipet is either 
carried under a stream of water and dried by a towel or all the 
urine is removed from its surface by a damp towel. 

2. This pipet, with its contained urine, is placed near the 
bottom of a bottle containing pure nitric acid, when the pressure 
of the index-finger is lessened and the acid allowed to flow gradu- 
ally up into the pipet (Fig. 83)^ 

3. When the pipet is seen to contain about the same amount 
of the acid and of the urine, the finger is again pressed firmly 





Fig. 83. 



-Method of filling lower portion of 
pipet with nitric acid. 



Fig. 84. — Pipet containing an upper 
stratum of urine, a lower stratum of 
nitromagnesium solution, and showing 
a white line (albumin ring) at zone of 
contact. 



upon the top of the pipet, which is then removed from the bottle 
and held toward the fight on a level with the eye; when, if al- 
bumin be present, a distinct white cloud in the form of a ring 
appears at the zone of junction of the urine and the reagent (Fig. 
84). The ring is often intensified by placing the pipet in different 
fights or against a dark background. The hand when placed 
back of the pipet and carried slowly above and then below the 
level of the ring serves this purpose. 

The time occupied in performing this test is very sfight, usually 



SERUM-ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 209 



only a few seconds. Its ease of execution, the fact that the albumin 
ring is not affected by the jarring of the pipet due to it being 
formed in a tube of small caliber, the small quantity of both urine 
and reagent needed, and the fact that it does away with the use 
of test-tubes, render this method of extreme practical value to 
both the general practitioner and the laboratory worker. 

At times it may be preferable to apply the nitric acid with the 
addition of heat, in which case the acid is placed in a test-tube 
and heated to the desired temperature; then a pipet containing 
the urine to be tested, as before described, is carried to the bottom 
of the tube and the acid allowed to slowly enter the pipet. The 
pressure of the index-finger 
should not be entirely removed 
until the acid has forced the 
column of urine up into the 
pipet, so as to make its superior 
surface on a plane above that 
of the acid occupying the space 
between the outer surface of the 
test-tube and the pipet (Fig. 85). 

By this method the urine and 
the reagent may be set aside and 
examined at intervals. The ring 
is not affected by returning the 
finger pressure at the top of the 
pipet and carrying the reacting 
specimen about the room for 
class demonstration. Through 
the courtesy of Prof. George H. 
Meeker, of the Medico-Chirur- 
gical College, I have been pro- 
vided with a testing pipet which 
serves well in this capacity. This method of keeping the nitric 
acid in contact with the urine for several hours is of special value 
in the estimation of uric acid, but it is necessary that the column 
of urine extend for fully two and one-half inches above the zone 
of contact. The ring caused by an excess of uric acid is less 
compact than the one produced by albumin, and always occurs 
high above the zone of contact. 

Appearance of the Reaction Ring and its Significance. — Here 
it is my object to elucidate as nearly as possible the value of 
the reaction obtained by the analysis of urines containing certain 
named substances; and an important fact in this connection is 
not to overestimate many of the less common of these reactions. 
14 




Fig. 85.— Test-tube containing- hot nitric 
acid, and pipet containing albuminous urine. 
White line (albumin ring) at zone of con- 
tact. 



2IO THE URINE. 

It is ever to be borne in mind that more than one substance 
capable of producing color and other changes may be present in 
the same urine, thereby confusing the results. The ring due to 
serum-albumin and other albuminoid bodies is fairly constant 
in its general characteristics, and comprises what the writer has 
been forced to accept, after five years of daily appHcation, as a 
most trustworthy test. 

Normal Urinary Pigments. — In highly colored urines a re- 
action may be detected at or near the zone of contact, which pro- 
duces a more or less distinct cloud, varying from a pink tint to a 
dull brick-red color. 

Serum- albumin. — When this body is present in quantities 
of pathologic moment the ring is seen at the zone of contact as a 
whitish band, the thickness of which varies in different specimens. 
Such variations are influenced (i) by allowing the acid to enter 
the pipet too rapidly, and (2) by the amount of albumin present 
in the specimen under observation. 

GlobuKn, albumoses, and peptones may also cause a small 
ring at the zone of contact. In the aggregate it may be said that 
the ring caused by these bodies is less clearly outhned by distinct 
margins characteristic of serum-albumin (see Alhumose and 
Peptone, pages 216, 217). The cloud of albumin may at times be 
slightly colored by the pigments present in the urine. This feature 
is most notable in connection with biliuria and hematuria. 

Mucin (N ticleo- album in) . — When present in sufficient amounts 
this produces a ring which resembles that of serum-albumin in 
color, but never presents a clear, pearly white tint, and, on the 
whole, this ring is less perfect than is that of serum-albumin 
even when of the same thickness; and, in striking contrast to 
albumin, it appears some distance above the zone of contact. 

Urates. — Urates may cause a distinct ring, varying in inten- 
sity from a slight reddish tinge to a deep cherry or brownish red. 
This ring occurs very near, but above, the zone of contact, and 
often requires close inspection to detect the thin zone of urine 
between the ring and the superior surface of the reagent. In 
some specimens the ring forms from one-eighth to one-half inch 
above the zone of contact. 

Biliuria. — Bile-pigments, when present in considerable amounts, 
cause a decided play of colors at the zone of contact. The ring 
of serum-albumin in such urines is apt to be colored, as is also 
the ring produced by mucin. After all known methods are em- 
ployed to remove these two bodies (albumin and mucin) from the 
urines, a decided reaction-ring still persists about one-quarter 
to one-half inch above the zone of contact. From these results 



SERUM- ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 211 

it would appear that nitric acid and the other contact reagents 
have not proved to be rehable tests for serum-albumin when 
in connection with bile-pigments. 

Indlcan. — Here, too, color changes are observed, which assume 
a violet hue and vary in intensity with the amount of indican 
present. The change is seen slightly above the zone of contact. 

Resinous Bodies. — These are usually precipitated by nitric 
acid, but seldom confuse the reaction for albumin. A further 
discourse by the author upon reagents may be found in the "New 
York Medical Journal," May 24, 1902. 

Quantitative Estimation of Albumin. — Heat. — Compara- 
tive results are to be obtained by boiling a given quantity of the 
urine which is acidified with acetic acid; and allow to stand for 
twenty-four hours in order that the albumin may collect at the 
bottom of the tube. A graduated tube may be employed for 
this purpose, but the ordinary test-tube gives fair results. The 
tube and its contents obtained from the first boiling may be corked 
tightly and set aside to be used for a comparison with the amount 
of precipitate that results from future tests; although a far better 
plan is to record the depth of sediment present at each examination. 
The albumin may at times separate out into large flakes, again 
into small flakes, and this in conjunction with other appreciable 
conditions causes the quantity of albumin to fluctuate greatly 
when estimated by this method. (It can be recommended, how- 
ever, to the general practitioner.) 

Volumetric Method. — This is by far the easiest method of 
execution and, therefore, deserves special mention. Take 10 
to 20 c.c. of the urine and to it add sufficient distilled water to 
make the total reach 50 c.c. Treat with two drops of a i per 
cent, aqueous solution of true yellow, and later titrate with a 25 
per cent, solution of salicyl-sulphonic acid until the mixture 
assumes a brick-red color. Multiply the number of cubic centi- 
meters of reagent employed by 0.01006, which will indicate the 
amount of albumin in the number of cubic centimeters of urine 
examined. Urine employed for this test should be acid in re- 
action. When alkaline, acidify with acetic acid. 

Esbach's Method. — This method for the estimation of the 
quantity of albumin is subject to rather decided variations and 
even liable to gross error; yet if all precautions herein outlined 
are observed, it will be found the most practical method now in 
vogue for the quantitative estimation of albumin. 

Reagents. — 

Picric acid lo gm. 

Citric acid 20 " 

Distilled water 1000 c.c. 



212 



THE URINE. 



A special tube (Fig. 86) is to be employed, and upon it will be 
found the letter U, indicating the portion of the tube to be filled 
with urine, and nearer the top of the tube is seen the letter R, which 
indicates the level to which the reagent is to be added. Beginning 
at the bottom of the tube is a scale graduated from i to 7. 





Fig. 86. — Esbach's albuminometer : 
A represents the author's brush for 
cleansing the albuminometer. In the 
actual brush the handle is about nine 
inches long. 



Fig. 87.— Receptacle for Esbach's albumin- 
ometer, devised by Dr. W. G. Mudie while 
working in the author's laboratory. In the 
bottom of an ordinary tumbler place a piece of 
heavy cardboard and cut central openings in 
two other cardboards which are glued in posi- 
tion. 



Process. — Fill the Esbach tube with filtered acid urine to U, 
and add the reagent until it reaches R. Then place the thumb 
over the mouth of the tube and invert it several times to insure a 
perfect mingling of the urine with the reagent. The tube should 



SERUM- ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 213 

now be placed in a special receptacle (Fig. 87) and allowed to 
stand for twenty-four hours, when the sediment which collects at 
the bottom of the tube will consist of serum-albumin, serum- 
globulin, albumoses, uric acid, and kreatinin. The amount of 
sediment is read directly from the scale, and indicates the amount 
pro mille in grams. 

Wetherill has designed the torfuge(p. 528,Fig. 233) so as to con- 
tain Esbach's albuminometer, and by the use of this instrument 
the reading may be obtained in from one to two minutes. 

Cautions. — Where the specific gravity of the urine is above 
1.008 the specimen should be diluted with water to reach this 
density. The temperature of the room should be 15° C. (59° F.). 
The urine must be acid. 

Different Densities. — The urinary albumin may be estimated 
by obtaining the specific gravity of the urine as voided, and after 
it has been freed from albumin. 

Application. — i. Treat a quantity of urine of known specific 
gravity with sufficient acetic acid to precipitate the albumin, and 
note the specific gravity. 

2. Place the solution in a rubber-stoppered bottle (the stopper 
having been previously boiled in sodium hydrate and washed to 
remove all alkali), tightly fasten it, and hold it in position by a 
wire. 

3. Place the bottle in boiling water for from ten to fifteen 
minutes. 

4. Cool and filter, guarding, as much as possible, against evapo- 
ration by passing the urine through a funnel surrounded by a 
closely fitting stopper, and by keeping the funnel covered with 
a glass plate. 

5. Ascertain the specific gravity of the filtered urine — it is 
best to employ a pyknometer. Multiply the decrease in specific 
gravity by 400 and the product equals the number of grams of 
albumin present in 100 c.c. of urine. 

Gravimetric Method. — i. Take 500 to 1000 c.c. of acid fil- 
tered urine (if alkahne, acidify with acetic acid) and place a 
few cubic centimeters of this quantity in a test-tube, heat in boiling 
water until coagulation occurs, heat again over a flame, and filter. 

2. Test the filtrate with acetic acid and potassium ferrocyanid. 
Should no precipitate form, treat the entire quantity of urine in 
the same manner, no further addition of acid being required. 

3. In the event of albumin being demonstrable with acetic 
acid and potassium ferrocyanid, the entire volume should be 
treated with a 30 per cent, solution of acetic acid (adding a few 
drops at a time) and stirring with a glass rod after each addition. 



214 THE URINE. 

4. After having proved that the urine is sufficiently acid to 
allow a complete precipitation of the albumin present, place 100 
c.c. or more in a rubber-stoppered bottle (see (2) Method of 
Different Densities), and first heat in boiling water until the 
albumin is seen to separate in flake-Hke particles. Then remove 
the bottle from the water, wipe dry, and again boil. 

5. Decant the supernatant urine, passing it through a dried, 
weighed filter, and later bring the entire precipitate upon the 
filter, care being taken to detach all particles of albumin that may 
cHng to the beaker by means of a glass rod tipped with rubber 
tubing and by washing with hot water. 

6. Wash the precipitate until the washings are no longer 
turbid, and treat with a drop of nitric acid and silver nitrate. 
Again wash with alcohol, and with ether remove all fats, after 
which the filter is dried at 120° to 130° C. (248° to 266° F.) and 
weighed. Should greater accuracy be required, incinerate the 
dried and weighed precipitate and thus determine the amount of 
mineral ash present with the albumin, and deduct this amount 
from the original weight. 

Whenever possible it is well either to dilute the urine suffi- 
ciently that not more than 0.2 to 0.3 gm. of albumin be contained 
in the quantity of urine employed, or to employ less than 100 c.c. 
of urine, thereby accomplishing this end. 

Serum-globulin. — Test. — i. Place from 20 to 50 c.c. of 
filtered urine in a beaker, and render it alkaline by adding ammo- 
nium hydrate. Phosphates are thus thrown out of the solution 
and should be separated by filtering. 

2. Add to the urine an equal quantity of a saturated solution 
of ammonium sulphate. A precipitate is indicative of the presence 
of globulin. Ammonium urate may also be separated from the 
solution, but is placarded by its color (see Ammonium Urate, 
page 272). 

Patents Test. — After the urine has been rendered alkaHne 
and the phosphates separated as previously outHned, place 10 c.c. 
of a saturated solution of sodium sulphate in a test-tube and allow 
some of the urine to flow in along the side of the tube so as to 
form a layer above the reagent. Serum-globuhn causes a white 
ring to appear at the zone of contact. 

Quantitative Estimation. — After serum-globuhn has been pre- 
cipitated by one of the methods described, allow the mixture 
to stand for one or more hours, collect the precipitate on a dried 
and weighed filter, and wash with a half-saturated solution of 
ammonium sulphate until the washing fails to give a precipitate, 
when treat with acetic acid and potassium ferrocyanid. Con- 
tinue as in the quantitative estimation of serum-albumin, page 211. 



SERUM- ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 21 5 

Mucin (Nucleo-albumin). — Nucleo-albumin differs from 
globulin in that it is insoluble in acetic acid. It is precipitated 
by magnesium sulphate, and does not form reducing substances 
when boiled with dilute acids, which also serve to distinguish it 
from true mucin. 

Place 10 c.c. of filtered urine in atest-tube and add concentrated 
acetic acid in excess — turbidity indicates the presence of nucleo- 
albumin. Should serum-albumin be present, it is to be removed by 
boiling and filtering, after which dilute the urine i to 3 of water, 
which prevents the possibility of turbidity resulting from urates, 
and lessens the power of the urinary salts to dissolve the mucin. 

Ott's Test. — Reagent. — Almen's solution: 

R . Tannic acid 5 gm. 

Sol. acetic acid (25 per cent.) 10 c.c. 

Alcohol (40 to 50 per cent.) 240 c.c. 

M. and keep in a glass-stoppered bottle. 

Place 10 c.c. of the filtered urine in a beaker and add an equal 
volume of a saturated solution of common salt. Shake well and 
then slowly add a small quantity of Almen's solution, when, should 
nucleo-albumin be present, a precipitate appears immediately. 

The following table may serve to differentiate between mucin, 
nucleo-albumin, and pus, though the two former of these bodies 
appear to be of questionable nature and have therefore been con- 
sidered under one head. 

Mucin. Nucleo-albumin. Pus. 

1. In acid urine mucin i. Spontaneous precip- i. Thick white or yel- 

forms a loose, whit- itate rare. Caused lowish-white precip- 

ish precipitate. by magnesium sul- itate in acid urine, 

phate. 

2. When urine is render- 2. Not influenced. 2. Unaltered. 

ed alkaline, precipi- 
tate is partially or 
entirely dissolved. 

3. Caustic potash causes 3. Slightly influenced. 3. Causes the precipitate 

no further change. to become stringy 

or ropy. 

4. Microscopic examina- 4. Negative. 4. Pus-cells showing vari- 

tion negative. ous stages of de- 

generation. 

5. Insoluble in excess of 5. Feebly soluble in large 5. Insoluble. 

acetic acid. excess. 

6. A diffuse or indistinct 6. A sharp ring at zone 6. An albumin ring the 

hazy band at zone of contact. rule. 

- of contact with nitric 
acid applied by Hel- 
ler's and the author's 
methods. 

7. Yields a reducing sub- 7. Does not yield reduc- 7. Unimportant. Does 

stance when boiled ing substances as a not contain phos- 

with mineral acids; rule. Its ash con- phorus. 

and its ash does not tains phosphorus. 
contain phosphorus. 



2l6 THE URINE. 

Clinical Significance. — Nucleo-albumin, or a substance closely 
allied to it, and mucin are normal constituents of the urine, and 
are to be found in large amounts during the course of catarrhal 
processes of the urinary tract, especially of the bladder. 

Emulsion-albuminuria. — Under this caption Cramer* has 
described a unique condition of the urine. In this condition 
the urine is chylous in appearance, but when placed under the 
microscope its turbidity is found to be due to a peculiar hazing 
of the entire field caused by innumerable minute globules of fat. 
When extracted with ether no fat is to be obtained and the osmic- 
acid reaction is negative. After the evaporation of the ethereal 
solution an almost colorless residue results, which in one instance — 
Coriat's case t — emitted an odor of burned sugar. Fehling's solu- 
tion gives a doubtful reaction, and Nylander's (bismuth) testis 
negative. There is no formation of an osazone with phenyl- 
hydrazin and sodium acetate (page 229). No volatile liquid is 
obtained by destructive distillation {acrolein test). The milkiness 
of such urine is changed to a mere opalescence upon the addition 
of a few drops of acetic acid or of potassium hydrate. Dilution 
of the urine with several times its own volume of water also 
causes a mere opalescence. 

Urine acidulated with hydrochloric acid and heated upon a 
water-bath for one hour may deposit a crystalline substance which 
is probably allantoin. This body appears to be more closely 
allied to crystalline globulin; the crystals occasionally found in 
urines containing Bence- Jones' albumose; and also the colloidal 
solution of metals, where, by electric pulverization of such 
metals as platinum, silver, and iridium, they become mechanically 
suspended as fine particles in water or other fluids. The urine 
partly cleared by dilution or otherwise gives the ordinary reactions 
for proteids. 

Upon boiling, a copious precipitate is obtained; the super- 
natant Hquid first becoming opalescent and eventually clear. 
Artificial peptic digestion also clears the urine; but it remains 
milky upon the addition of hydrochloric acid alone. 

Microscopy. — The sediment of such urine is Hkely to contain 
crystals of uric acid, amorphous urates (few), leukocytes, and in 
one instance pus and a few erythrocytes were found. 

Thus far I have been able to recover from the literature re- 
ports of but four examples of emulsion-albuminuria. 

Albumoses. — Acidify 10 to 20 c.c. of urine with acetic acid 
and to it add a saturated solution of sodium chlorid, and shake. 

* " Miinchener med. Wochensch.," Jan. 21, 1902. 
t "Med. Rec," Nov. 14, 1903. 



SERUM- ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 21 7 

Albumoses cause a precipitate to appear upon gentle application 
of heat before the boiling-point is reached, but should ebulHtion 
be prolonged, this precipitate is dissolved in part or in its entirety, 
to reappear on coohng; and when filtered hot, the filtrate becomes 
cloudy on cooling. Render the hot filtrate alkaline with sodium 
hydrate and to it add, drop by drop, a i per cent, solution of 
copper sulphate; continue to heat, and a red color develops (biuret 
reaction). 

Millon's Reaction. — MiUon's Reagent. — 

Mercury i part 

Nitric acid (specific gravity 1.42) 2 parts 

Distilled water 6 " 

Place 10 c.c. of urine in a test-tube and to it add a small quan- 
tity of Miilon's reagent ; boil briskly and a red color develops. 
(Allusion to further tests for albumoses is made under Serum- 
albumin, page 210, and in connection with Bence- Jones' albu- 
mose, page 218.) 

Peptones. — Peptones, in the opinion of Kiihne, do not occur 
in the urine, but the substance generally regarded as peptone is 
classified under this caption for want of a more appropriate term. 

Test. — SalkowskPs Method. — i. Place 50 c.c. of the urine in 
a beaker and acidify with 5 c.c. of hydrochloric acid; add 
phosphotungstic acid, heating over a flame for five minutes, when 
a precipitate will collect in the form of a resinous mass adhering 
closely to the bottom of the beaker. 

2. Decant supernatant fluid, wash the precipitated mass twice 
with distilled water, decanting after each washing. 

3. Add to the precipitate 8 c.c. of distilled water and 0.5 c.c. 
of sodium-hydrate solution (specific gravity 1.16). Upon shaking 
the beaker and stirring the mass with a glass rod it is readily 
dissolved, and the solution assumes a dark-blue color. 

4. Heat over the flame for several minutes, when the blue 
color is replaced by a dirty grayish yellow, and the solution 
becomes turbid, though rarely it remains clear. At this point 
place a few cubic centimeters of the solution in a test-tube, cool, 
and treat with a i per cent, solution of copper sulphate (drop by 
drop) when a bright-red color (biuret reaction) appears. Albumin 
and mucin should be removed from the urine (see page 206), 
though the latter substance seldom interferes with the reaction. 
By this method 0.015 E^- of peptone per 100 c.c. may be readily 
demonstrated. 

The biuret reaction is hkewise obtained with the urine of 
pneumonia and other febrile conditions. When question arises, 



2l8 THE URINE. 

not more than lo c.c. of urine should be employed for the reaction. 
Hematoporphyrin (page 223) will be found to interfere with this 
reaction, in which case the urine must be precipitated by barium 
chlorid, an alcoholic extract obtained, and the filtrate, w^hich 
holds in suspension the albumoses, examined. 

Clinical Significance. — Peptone may appear in the urine 
as a result of pathologic conditions, and its presence is probably 
dependent upon the decomposition of organized proteids, except 
in cases of the enterogenic form (constipation). It may owe its 
origin pathologically to the action of bacteria upon the tissues, 
or to chemic poisons (phosphorus), and it may be encountered 
with the various cirrhoses of the liver, acute yellow atrophy, gas- 
tric cancer, gangrene, acute or chronic suppuration, acute inflam- 
mation of serous surfaces, leukocythemia, infectious fevers, after 
death of fetus, and physiologically during involution of the uterus. 

Bence- Jones' Albumose. — This form of albumosuria, though 
extremely rare, is doubtless worthy of special consideration, and 
it is the author's belief that a more definite knowledge of the 
reactions common to this body will facilitate its recognition, 
thereby elucidating a number of obscure conditions. Since the 
original report of Henry Bence- Jones, there have appeared in 
the Hterature, from time to time, reports of thirty-five cases of 
Bence- Jones' albumosuria; four of these having been studied 
by the author.* 

Tests. — I. Place from 10 to 20 c.c. of filtered urine in a test- 
tube and heat, allowing the flame to warm the upper stratum of 
the urine. Bence- Jones' albumose causes an opalescence to 
appear long before the boihng-point is reached, and when near 
the boiling-point, the fluid becomes opaque, and coarse flocculi 
are seen falHng to the stratum of unheated urine. When the 
boihng-point is reached this turbidity will be seen to diminish 
sHghtly. When ebullition is prolonged for from one to three 
minutes, a portion and, sometimes, nearly all the turbidity dis- 
appears ; but upon standing the tube aside and allowing the urine 
to cool, this clouding reappears and is often more pronounced than 
before the boihng-point was reached. 

2. Place from 10 to 40 c.c. of the filtered urine in a beaker 
and heat over a water-bath, keeping careful watch at what tem- 
perature the opalescence is observed. Bence- Jones' albumose causes 
a slight cloud at 52° C. (125.6° F.), and at 54° to 56° C. (129.2° 
to 132.8° F.) a marked turbidity appears, which develops into a 
dense cloud at from 56° to 60° C. (132.8° to 140° F.). A rather 

* Phila. Col. Physicians, June 4, 1902; Anders and Boston, " Lancet," Jan. 10, 
1903; "Amer. Jour. Med. Sci.," April, 1903. 



SERUM- ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 219 

tough coagulum formed in one urine examined when heated 
from 60° to 90° C. (140° to 194° F.). According to some writers, 
the addition of a few drops of acetic acid to the urine may cause 
the opalescence to appear at a lower temperature (37° C. or 98.6° 
F.), though this has not been my experience. The coagulum 
or precipitate, however dense, will be found to dissolve in part 
when kept from two to six minutes at a temperature of 95° to 
100° C. boihng. 

3. Upon the addition of concentrated nitric acid, drop by drop, 
to the urine, the upper one-third of which has been gently heated, 
a precipitate appears in the track of the acid as it travels through 
the cold stratum of the urine to the bottom, where after the ad- 
dition of several drops, a rather dense precipitate of a sHght pink 
or yellowish hue collects. In some specimens this precipitate 
upon standing becomes a golden color. 

4. Add to the urine nitric acid, drop by drop, shaking after 
each additional drop, when a sHght pinkish tint appears affecting 
mostly the heated portion of the urine. 

5. Place 20 c.c. of urine in a test-tube, acidulate with acetic 
acid, and heat gradually to the boihng-point, cool, and filter. The 
filtrate thus obtained apparently contains but httle proteid, dis- 
playing a sHght opalescence with acetic acid, but no precipitate 
appearing with nitric acid. Nitric acid when added to such 
filtrate may lend a pinkish tint to the fluid, which upon the ad- 
dition of ammonia often assumes a yellowish shade. 

6. Place 50 c.c. of the urine in a beaker, heat over a water- 
bath to 54° C. (129.2° F.), and filter. Dissolve the precipitate that 
collects on the filter by washing with a solution of caustic soda (30 
per cent.); and then test for Millon's and the biuret reactions 
(Millon and biuret tests, page 217). 

7. This precipitate when heated with lead acetate (i per 
cent, solution) and caustic soda (30 per cent.) first displays sHght 
browning, but after the boiling has been prolonged for one or 
more minutes, the color gradually deepens to a dull black due to 
the formation of lead sulphid. Matthes, Milroy, Magnus Levy, 
and Huppert regard this reaction as dependent upon the fact that 
the precipitate contains sulphur (loosely combined) in considerable 
amount and as one of the most characteristic features of Bence- 
Jones' albumose. 

Saturation with Neutral Salts. — i. Place a quantity of filtered 
urine in a beaker and to it add an equal volume of neutral solu- 
tion of ammonium sulphate which will be found completely to 
precipitate the albumose. 

2. Saturation with sodium chlorid (equal volume) in neutral 



2 20 THE URINE. 

solution causes a precipitate of but a portion of the albumose; 
the filtrate clouding decidedly upon the addition of a small quan- 
tity of dilute acetic acid; but the filtrate from this second pre- 
cipitate does not contain albumose. Bence-Jones' albumose 
difi'ers from proto-albumose and hetero-albumose in that it is not 
completely precipitated with sodium chlorid in neutral solution. 
It resembles hetero-albumose in that it is precipitated on the 
addition of acetic acid after saturation with sodium chlorid or 
magnesium sulphate, but differs from this body in being precipi- 
tated at a temperature of 52° C. (125.6° F.). 

Bence-Jones' albumose is precipitated by sulphuric, hydro- 
chloric, tannic, and picric acids. Reactions 5 and 6 will be found 
equally decisive after the urine has been saturated with neutral 
salt. Place 50 c.c. of the filtrate thus obtained, which contains 
albumose, in a beaker and add a drop of hydrochloric acid; stir 
gently, after which a few drops of phosphotungstic acid should 
be added and heat gradually applied, which when prolonged for 
a few minutes causes a copious precipitate to collect at the bottom 
in the form of a rather tough, whitish mass. Decant the clear 
supernatant fluid, and dissolve this precipitate in a 30 per cent, 
solution of caustic soda, adding drop by drop. This usually 
gives a colorless mixture, but occasionally it will be found to 
display a blue or purple tint, which disappears when the specimen 
is gently heated. 

Special Tests. — The Millon, biuret (page 217), and sulphur 
reactions may now be continued as described under 5 and 6. 
Kiihne and Alatthes found Bence-Jones' albumose to contain 
phophorus in rather large amounts, while IMilroy was unable to 
recover phosphorus in his studies. Simon has subjected this body 
to peptic digestion. 

Histon. — Bence-Jones' albumose resembles in many respects 
histon, which under certain conditions may be derived from 
nucleo-histon, a proteid of the leukocytes. Milroy regards histon 
to be an intermediate between albumin and albumose. Histon 
is precipitated from acid solutions by ammonia, while albumose 
causes no precipitate. Histon when heated yields a precipitate 
which is soluble in dilute acids. It is precipitated on the addi- 
tion of nitric acid; this precipitate disappearing when heated to 
the boihng-point, to reappear on cooHng. It gives a decided 
rose-pink color with copper sulphate and caustic soda (biuret). 

Glohin. — Shultz and Milroy have studied correlatively the 
reactions for Bence-Jones' albumose and for globin, and found these 
bodies to behave alike when treated with strong hydrochloric and 
nitric acids, and also to give the biuret reaction. Albumose gives a 



SERUM- ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 2 21 

distinct red with Millon's reagent, globin a pink; and albumose 
contains loosely combined sulphur. Globin when precipitated 
by heat is readily soluble in dilute acids, a feature less prominent 
in albumose. 

Clinical Significance and Peculiarities. — Bence- Jones' albu- 
mosuria is a condition which manifests itself after the age 
of twenty years. Males are affected in 80 per cent, of the cases. 
In 15 per cent, of cases there is a history of traumatism inflicting 
severe injury to the bony skeleton. Primary lesions of the bones 
(myeloma) have been found postmortem in 80 per cent, of cases. 

This condition (albumosuria) may be persistent, transitory, 
or, less commonly, remittent, occurring in variable degrees at 
different hours during the day. The specific gravity of the urine 
may fluctuate between 1.002 and 1.040, and there appear records 
of six instances where the urine resembled syrup. The color of 
the urine varies greatly. The quantity for the twenty-four hours 
is usually normal, though polyuria may develop. 

Maladies displaying albumosuria are usually fatal in from 
one to two and one-half years. 

Hematuria. — Hematuria is a condition wherein the cellular 
elements of the blood escape through the urine, giving to this 
secretion a bloody color which upon standing becomes of a more 
or less blackish or brownish red, and at the bottom of the Hquid 
there is seen a chocolate precipitate containing blood-cells and 
often blood crystals. The reaction of the urine modifies the 
microscopic character of the precipitate. 

Heller's Test. — This test depends upon the presence of blood- 
pigment and therefore gives a positive reaction with both 
hematuric and hemoglobinuric urines. Place a test-tube in urine 
to the height of two inches and render strongly alkaline with caustic 
soda (30 per cent.), after which boil. Blood- pigment gives a 
brownish-red deposit, while the supernatant fluid becomes bottle- 
green. This precipitate consists of earthy phosphates and hematin 
derived from the blood-pigment present, and is therefore reddish 
in color instead of being white or yellow as would be the case were 
only phosphates deposited. Alkaline urine should first be treated 
with a few drops of calcium-chlorid solution. When the color 
of the urine is very dark, due to the presence of pigments of blood 
or bile, decant the supernatant fluid and add to the precipitate 
an equal volume of water. This test is capable of detecting i 
c.c. of blood in i Hter of urine. 

Fallacies. — When the patient is taking senna, santonin, or 
rhubarb, a positive reaction is obtained with the urine in the 
absence of blood-pigments and it is necessary to resort to spectro- 



222 THE URINE. 

scopic analysis to distinguish between these reactions and that 
of blood. 

Hemoglobinuria. — Hemoglobinuria is a condition marked 
by the presence of hemoglobin or its derivative, methemoglobin, 
in the urine without the presence of red blood-cells, and is excited 
by the conditions capable of inducing hemoglobinemia (page 
141), among which malaria deserves special mention. It may 
occur where the urine shows a small number of red cells micro- 
scopically, the urine containing hemoglobin whenever the red 
cells are present in sufficient numbers. The specific gravity of 
such urines is commonly low (1.008), but in exceptional instances 
it may reach 1.030. Bloody urine is turbid and therefore pla- 
carded by its color, which may vary from a bright red to almost 
a black. Oxyhemoglobin can be recognized as such by the 
spectroscope, since it gives rise to the appearance of two absorp- 
tion-bands located between D and E (Fig. 24). 

Microscopically, red blood-cells are rarely present. The field 
contains much granular debris, among which are seen many small 
droplets which are often of a yellowish color. Coarse clusters of 
yellowish matter are to be seen, as are also crystals of hematoidin 
(Plate 17) and epithelial cells containing granules of pigment. 

Spectrum. — Render a quantity of the suspected urine acid 
by adding a few drops of acetic acid, place in a test-tube, and hold 
before the open sHt of the spectroscope, when the bands of oxy- 
hemoglobin will be seen. Should these bands not appear at 
once, dilute the urine with distilled water until they become per- 
ceptible. Add a few drops of ammonium sulphid to the urine 
and the spectrum is converted to that of reduced hemoglobin. 
In my own experience it has been common to obtain a spec- 
trum of reduced hemoglobin (Fig. 24) in cases of hemoglobinuria. 

Guaiacum Test. — Place one inch of urine in a test-tube and 
allow a mixture of equal parts of tincture of guaiacum and oil of 
turpentine that has been ozonized by exposure to the air to flow 
from the pipet along the side of the test-tube so as to form a dis- 
tinct layer upon the urine. Blood-pigment causes a white ring 
to appear at the zone of contact, which soon changes to a blue, due 
to oxidation of the guaiac by oxygen derived from the ozonic ether, 
the blood-pigment acting as a carrier. (Ozonic ether is a solution 
of peroxid of hydrogen in sulphuric ether.) 

Fallacies. — Should the urine contain iodids, the blue color also 
appears with this test and is to be distinguished from the reaction 
due to blood by the fact that the color appears much more slowly 
and in addition develops simultaneously throughout the fluid 
instead of at the junction of the urine and the ether. In the pres- 
ence of pus a greenish-blue color appears, but the urine is decolor- 



SERUM-ALBUMIN AND SERUM-GLOBULIN IN THE URINE. 223 

ized on heating. Where the urine has been voided in a vessel into 
which sputum has been collected, saliva will be found to cause 
tliis reaction with guaiacum. 

Methemoglobinuria. — Methemoglobin is a derivative of the 
blood which may be formed from hemoglobin, in acid urine, after 
it has been allowed to stand for several hours; and it is not un- 
common to find methemoglobin in the freshly voided urine. 
CKnically it has been regarded as indicative of renal hemorrhage. 
The urine has a smoky tint, and upon spectroscopic study (see 
Blood, page 45) furnishes the only satisfactory test for methemoglo- 
bin. For this purpose it is well to filter, and also to dilute, the urine. 

Hematoporphyrinuria. — Iron-free pigment (hematin) occurs 
normally in the urine, though in but minute amounts, and may 
be considerably increased without noticeably altering the color 
of the urine, while in hematoporphyrinuria the urine has a port- 
wine color and does not give the guaiac reaction. Spectroscopic- 
ally, when studied in a thin layer, it may show a characteristic 
spectrum of the so-called "alkaline hematoporphyrin" (Fig. 24), 
and in this way may be encountered in acid urines. It is not un- 
common, however, for spectroscopic study to yield negative re- 
sults, and in such instances the pigment can be extracted by 
shaking the urine with a small amount of amylic alcohol or acetic 
ether, after the addition of one or two drops of acetic acid. The 
extract thus obtained when studied spectroscopically reveals the 
bands of alkaline hematoporphyrin, which are four in number: 
one at the junction of the red and yellow between C and D, a 
second in the yellow, a third in the green both between D and 
E, and a fourth, darkest and broadest, appearing between E 
and F, and the green and the blue (see Fig. 24). The bands of 
hematoporphyrin may be obtained by the addition of one or more 
drops of hydrochloric acid, and are two in number: one narrow 
band in the orange between C and D, and another broader band 
at the junction of the yellow and the green between D and E, 
which is the characteristic band. In reality this consists of two 
halves, a lighter, situated nearest the narrow band and a very 
dark, located half way from it. 

Clinical Significance. — Hematoporphyrin may appear in 
large amounts in the urine of persons who have been taking 
sulphonal.* It is said to be more common in females than in 
males and should be regarded as a grave symptom. 

Histon. — Collect the product of twenty- four hours and examine 
first for serum-albumiin and albumose, as has been previously 
outlined (page 200). Precipitate the histon with from 90 to 94 

* Tyson and Croftan, "Phila. Med. Jour.," May 17, 1902, p. 882. 



224 THE URINE. 

per cent, alcohol, and wash the precipitate with hot alcohol and 
dissolve in boihng water; cool, acidify with a few drops of hydro- 
chloric acid, and set aside for several hours. During this time 
clouding and decided precipitate appear, composed largely of 
uric acid (which has to be separated by filtration), and the filtrate, 
precipitated with ammonia, which throws out of solution histon 
and certain other constituents of the urine. Collect the precipitate 
on a filter, and wash with ammoniacal water until the wash- water 
fails to give the biuret reaction. Dissolve the precipitate in dilute 
acetic acid and test the solution for the biuret reaction. Should 
this be positive and coagulation occur upon the application of 
heat, and the coagulum be soluble in mineral acids, histon is 
probably present (see Differential Points jor Histon and Bence- 
Jones^ Albumose, page 220). 

Fibrin. — Fibrin may occur in the urine in the form of rather 
decided clots, and their character is quite distinct after thorough 
washing with water. Clots of fibrin are dissolved by boiling in 
a I per cent, solution of soda or in a 5 per cent, solution of hydro- 
chloric acid. After the dissolution of these fibrinous coagula, 
test the urine for serumx-albumin (page 206). 



CARBOHYDRATE (SUGAR) IN THE URINE. 

The sugars that occur in the urine which are of practical im- 
portance from a cHnical point of view are glucose and lactose. 
It is possible, however, that levulose sometimes occurs in con- 
junction with glucose, and cane-sugar and maltose may appear 
in the urine after the ingestion of a large amount of either of these 
substances. Their occurrence is commonly described under the 
special caption of pentoses (page 238). Their clinical importance 
is at present undetermined. 

GLUCOSE. 

Glucose (dextrose or grape-sugar, C^^H^fi^) forms by far 
the commonest variety of sugar encountered in the urine, and its 
presence there is commonly referred to as "glucosuria," yet 
properly speaking glucosuria is not true diabetes melHtus unless 
glucosuria forms the most conspicuous feature of the condition. 
A mere trace of glucose may be met with in normal urine, but not 
in sufficient amounts to render it capable of detection by the 
reagents commonly employed for this purpose. Therefore, 
whenever a reaction for glucose is obtained by our present labora- 
tory methods, a pathologic glucosuria exists. 

Clinical Significance. — Glucosuria may be persistent or 



GLUCOSE. 225 

transitory, the latter form of which will be divided into three 
classes for the convenience of study. 

Transitory Glucosuria. — It is quite impossible within the scope 
of this volume to discuss in detail the various forms of transitory 
glucosuria, and therefore mere allusions to such conditions will 
be made. As previously stated, there is a faint trace of glucose 
in normal urine, and it has been further found that after breakfast, 
if the meal be rich in carbohydrates, sugar is usually demon- 
strable in the urine. In addition to diabetes mellitus, the causal 
factors of which are not herein discussed, there are to be encoun- 
tered the so-called ahmentary glucosurias, and in certain low-grade 
conditions transitory glucosuria is not an unusual occurrence. 
For convenience of study these transitory glucosurias may be 
classified under the following subheadings: (a) toxic; (b) those 
associated with disease or injuries to the human organism; and 
(c) puerperal glucosuria. 

Toxic glucosuria is to be seen after the administration of 
hydrochloric acid, sulphuric acid, mercury, strychnin, glycerin, 
alcohol, nitrobenzol, lead, arsenic, phosphorus, potassium iodid, 
caffein, thyroid extract, tubercuHn, pancreatin, phloridzin, diuretin, 
carbon monoxid, and morphin. Analgesics and anesthetics also 
possess the power of exciting transitory glucosuria, and several 
instances are recorded where glucosuria has followed the admin- 
istration of chloral, chloroform, and amyl nitrite; and three 
observers have found small quantities of sugar in the urine after 
ether anesthesia, while Andral reports a case of true diabetes 
developing after ether anesthesia. 

When the urine is capable of reducing copper after the ad- 
ministration of any of the above-named drugs, the phenylhydrazin 
test should be employed, as there are likely to be other reducing 
agents present in such urines. 

Among the pathologic conditions wherein transitory glucosuria 
has been detected should be mentioned cerebrospinal menin- 
gitis, in which disease I have found it to be of a rather common 
occurrence; cholera, relapsing fever, typhoid fever, diphtheria 
(in which I have seen two instances), phthisis, certain of the 
exanthemata, as scarlet fever, hepatic cirrhosis, rickets, gas- 
tritis, during malarial paroxysms, scarlatinal nephritis, chronic 
interstitial nephritis, choleHthiasis, syphilis, asthma, whooping- 
cough, and, according to the late Da Costa, in old age. Again, 
glucosuria may follow injuries to the cerebrospinal system and 
cerebral or pontine hemorrhage, traumatism to the head, cerebral 
abscess or tumor. It may occur in disseminated sclerosis, epi- 
lepsy, neuralgias, sciatica, and the various forms of insanity. It 
15 



226 THE URINE. 

has also been observed during the course of exophthalmic goiter, 
myxedema, and neurasthenia; as well as following traumatic 
neuroses, physical derangements, and anxiety or sudden emo- 
tions. The term functional glucosuria has been appHed w^here 
glucosuria develops in connection with many of these conditions, 
but in all instances it is Kable to be transitory in nature. 

Puerperal lactosuria is much more common than is glucosuria, 
although the latter condition is but rarely seen (see Lactosuria^ 
page 238). This form may possibly be toxic, although it is physio- 
logic unless the quantity of sugar be large. Roque* suggests 
the following classification of glucosuria: 

Intermittent glucosuria 0} arthritis, w^hich should probably be 
included with hereditary glucosuria of the young, as well as that 
of gouty adults and obesity. 

Digestive glucosuria is simply recognized by its disappearance 
after the withdrawal of carbohydrates from the diet and the 
removing of digestive disturbances. 

Nervous glucosuria, including those conditions associated with 
systemic affections involving the nervous system, neuroses, psy- 
choses, and traumatism. 

Tests for Glucosuria. — Many of the tests for glucose depend 
upon the fact that these substances become oxidized by the ex- 
penditure of certain metalhc oxids; such oxidation occurring 
easily at a temperature near the boiHng-point and in the presence 
of a free caustic alkaU. Copper serves as the most suitable metal 
for this test. Take a solution of caustic soda and to it add a few 
drops of a very dilute solution of sulphate of copper — a blue pre- 
cipitate develops which is hydrated cupric oxid (CUOH2O). Upon 
boihng, this blue precipitate changes to black from the separation 
of cupric oxid (CuO). When in the presence of certain substances, 
such as tartrate, the cupric hydrate pre\iously formed on the 
addition of the sulphate is retained in solution instead of being 
precipitated, and gives the fluid a deep blue color which is un- 
altered by boihng. In the presence of oxidizable substances, as 
glucose, the blue cupric hydrate is reduced, when the temperature 
is raised to near the boihng-point, to form cuprous hydrate (CU2- 
OH2O), which when thrown out of the solution appears as a yellow 
precipitate; or should it be further dehydrated, cuprous oxid 
(CuO) forms, which is red. 

Caution. — The solution containing glucose when rendered 
alkaline with caustic soda and treated with a few drops of cupric- 
sulphate solution causes cupric hydrate to be formed, which may 
be dissolved and the blue solution remain unchanged, but when 

* Paris, 1899. 



GLUCOSE. 227 

heated to the boiling-point glucose reduces the cupric hydrate 
and the yellow cuprous hydrate or the red cuprous oxid appears 
as a precipitate. 

Fehling's Test. — Reagents. — Solution I: Powder 34.64 gm. 
of pure crystallized sulphate of copper, and dissolve in 200 c.c. 
of warm distilled water; cool, and add distilled water to make 
500 c.c. 

Solution II : 

Crystallized Rochelle salts i8o gm. 

Distilled water (hot) 300 c.c. 

filter, and add 70 gm. of pure caustic soda ; cool, adding sufficient 
water to make 500 c.c. The solutions should be kept in colored 
glass-stoppered bottles. 

Preparation of Urine. — I. Place 10 c.c. of urine in a beaker, 
boil, and without removing any precipitate add to it 5 c.c. of the 
copper- sulphate solution used in preparing Fehling's solution, and 
after cooling add 0.5 c.c. of a saturated solution of sodium acetate 
which contains sufficient acetic acid to give to the mixture a rather 
feeble acid reaction. Filter. Employ the filtrate in testing with 
FehHng's solution as outlined below. The urine must be freed 
from albumin, and it is well to add a few drops of acetic acid; 
boil and filter, after which neutralize the filtrate with calcium 
carbonate. 

II. Fehling's test is not applicable to ammoniacal urine, as 
the free ammonium may prevent the precipitation of cuprous oxid. 
When the glucose present is more than necessary for the reduction 
of all the cupric oxid, the remaining glucose, should ebullition be 
prolonged, is liable to be caramelized, in which case both the 
liquid and the precipitate assume a dark brownish color. Mix 
equal volumes of solution (I) and (II) which results in an alkaline 
solution of potassic xupric tartrate, i c.c. of which is reduced by 
5 mgm. of pure glucose. When preparing for qualitative analysis 
add to this mixture three times its volume of water, which will 
result in a pale-blue solution. 

III. Fill a test-tube two-thirds full with the diluted Fehling's 
reagent, and boil the upper portion of the reagent for one minute. 
If the reagent remains clear it is fit for use, but should the slightest 
turbjdity ensue, its employment is unsafe, and caustic soda should 
be added to the solution, after which filtration is necessary before 
use. 

IV. Grasp the tube containing the reagent between the thumb 
and finger (see Plate 14), and heat the upper portion of the liquid 
over a free flame, at the same time adding, drop by drop, urine 



228 THE URIXE. 

from a pipet, and heating after each additional drop of the sus- 
pected alhumin-jree urine. In the presence of a considerable 
quantity of glucose, a yellow or red precipitate suddenly develops, 
its color changing gradually according to the quantity of glucose 
present, as well as to the dilution of the copper solution and the 
presence of other substances, such as uric acid and kreatinin. 
From 5 to 20 drops are sufficient to cause a reduction of the copper 
when glucose is present in pathologic amounts, yet more urine is 
often required. As the reduction develops, sm.all drops of the 
urine mil be seen falHng from the under surface of the reaction 
(precipitate) through the clear reagent and will cause a precipitate 
to form in the track of the urine as it traverses the reagent toward 
the bottom of the tube (Plate 14). This occurs only when glucose 
is present in considerable amounts, but when seen is a most char- 
acteristic feature. Such reactions after standing for a time are 
likely to show a diminishing of the yellow precipitate suspended 
near the top of the tube, while at the bottom a rather coarsely 
granular sediment collects (Plate 14). 

Cautions. — Never boil the upper portion of the urine briskly 
and do not heat the lower portion, since boihng obscures the 
characteristic features of the reaction, and renders the significance 
of the copper reaction questionable. Should no decoloration of 
the copper solution follow the addition of the urine, continue 
until the quantity of the urine that has been added nearly equals 
in volume that of the reagent. Boil gently for a few seconds and 
set aside. If upon cooling no precipitate develops, sugar is absent. 
When the precipitate develops late, the liquid first shows shght 
clouding and passes through the various stages from a clear bluish 
green to a light-green color, which often appears milky and is by 
some authors regarded as rather characteristic of dextrose, though 
it is more Hkely the result of some additional substance which 
interferes with the characteristic reaction. Fehling's test is capa- 
ble of detecting 0.8 per cent, of glucose, in which- case the pre- 
cipitate is yellow or red, but the color does not form until the liquid 
cools. 

Other Substances. — Copper is capable of being reduced by 
uric acid, kreatinin, calcium oxalate, and hippuric acid, all of 
w^hich are constituents of normal urine (and among abnormal 
ingredients are to be mentioned lactose, glycuronic acid, glycosuric 
acid), and following the administration of such drugs as chloro- 
form, chloral, benzoic acid, salicyHc acid, potassium iodid, 
saHcylates, glycerin, and carbolic acid (see Alkaptonuria, page 
247). When the precautions previously set forth have been ob- 
served, there are but two substances likely to confuse the reac- 



PLATE 14. 




Feeling's Test. 

I. Method of applying heat when using Fehhng's reagent; note the lower 
surface of the reaction. 2. Showing the result of standing. 



GLUCOSE. 229 

tions for glucose, viz., glycuronic acid and lactose, a point to be 
determined by the following tests: 

Nylander's or Bottger^s Test. — This reaction depends upon 
the power of glucose to reduce the bismuth compounds when in 
alkahne solution, with the formation of the black suboxid. 

Reagent, — Dissolve 10 gm. of caustic soda in 90 c.c. of warm 
water, and add 4 gm. of sodiopotassium tartrate and 2 gm. of 
bismuth subnitrate. After shaking thoroughly a hydrated oxid 
of bismuth is formed and is held in solution by the tartrate. Boil, 
filter, and keep in a glass-stoppered amber bottle. Place 10 
c.c. of urine in a test-tube and to it add i c.c. of the reagent, 
shaking sufficiently to cause a thorough mingling of the reagent 
through the urine; then boil over a flame for from one to three 
minutes. Sugar causes at first a brown and later a black pre- 
cipitate of bismuthous oxid (metalHc bismuth) to be thrown 
down. This reaction, while extremely dehcate, is less liable to 
occur with the substances normally found in the urine, and men- 
tioned under Fehling's test. It does occur as the result of gly- 
curonic acid, lactose, after the administration of rhubarb, salol, 
antipyrin, senna, and turpentine; and when urine contains an 
abundance of oxalate of calcium, a dark-brown precipitate is 
produced. Urines containing traces of sulphur also give this 
reaction, and albumins favor the precipitation of the black sulphid 
of bismuth. 

Picric-acid Test. — Place 10 c.c. of urine in a test-tube and 
to it add one-fourth its volume of a standard solution of picric 
acid; shake, and heat after adding a few drops of caustic potash. 
In the presence of sugar the solution assumes a dark-red color 
which is dependent upon the conversion of picric to picramic acid. 

Caution. — The kreatinin contained in normal urine may cause 
some darkening of the fluid, but the color does not resemble that 
produced by sugar, and the solution, while colored, does not be- 
come cloudy. Any impurity of the reagent may show spontaneous 
darkening when heated with caustic potash. 

Phenylhydrazin. — Place in a beaker one-half gm. of phenyl- 
hydrazin hydrochlorate (colorless crystals) and ij gm. of sodium 
acetate with sufficient water to dissolve, with the aid of gentle 
heat over a water-bath; then to this solution add 5 c.c. of the 
suspected urine and boil the mixture for from three to five minutes; 
after which set aside and cool. Should sugar be present the 
crystals will soon accumulate at the bottom of the liquid. A 
step which I prefer is to centrifugate some of this urine in order 
to recover the crystals for microscopic study. These crystals of 
phenylglucosazone appear as small needles, are of a bright yellow 



230 



THE URINE. 



color, and may appear singly, though commonly tend to congre- 
gate in rather dense aggregations, often arranging themselves in 
bundles, sheaves, stars, and fans. They are seen with a one- 
sixth lens. The phenylhydrazin test is sufficiently delicate for 
the demonstration of o.oi per cent, of glucose. The melting- 
point of phenylglucosazone is 205° C. (401° F.), while maltosazone 
melts at 190° to 191° C. (374° to 375.8° F.). 

Caution. — Maltose and certain pentoses are also capable of 
causing the formation of osazone. Crystals of lactose are, as a 
rule, short, heavy, and pointed at both extremities, and unless 
the sediment be centrifugated, show little tendency to form 
aggregations. 

Rigler's Test. — Place one and one-half gm. of pure phenyl- 
hydrazin crystals and 7 gm. of sodium acetate in a porcelain 
capsule, and boil after adding 20 drops of 
the suspected urine. Remove the capsule 
to the table and add 20 to 30 drops of a solu- 
tion of caustic soda (10 per cent.). In the 
presence of suga^ a red- violet color appears 
within one minute. 

Quantitative Estimation of Sugar. — 
Methods to be employed for the quantita- 
tive estimation of sugar are of necessity 
based upon the principles set forth in the 
qualitative tests previously outlined. 

Fermentation Test. — This test, while 
sufficiently reliable to justify its use, is not 
practical for general laboratory work and is 
not, therefore, employed to the exclusion of 
Fehling's test. Neither can it be said to be absolutely reliable, 
though possibly it is sHghtly more so than is Fehling's reaction. 

Take a quantity of the suspected urine, and render it acid by 
the addition of tartaric acid, after which it should be boiled for 
several minutes. When the urine is rich in glucose it is necessary 
to dilute it from four to ten or more times. The yeast to be 
employed must be fresh, and should have been tested in order to 
be certain that it possesses life. Rub up a portion of a cake of 
yeast (a piece about one-eighth inch square), mix it with the 
urine so as to form an emulsion free from lumps, and place the 
mixture in an Einhorn saccharimeter (Fig. 89). 

Direction. — Pour the urine from the beaker into the sacchar- 
imeter until the expanded portion is nearly filled ; then place the 
thumb over the mouth of the apparatus and incline the tube so 
as to cause the urine-yeast mixture to fill the graduated portion 




Fig. 89. — Einhorn's sac 
charimeter. 



GLUCOSE. 231 

completely, after which there will still remain some of the mixture 
in the expanded portion of the saccharimeter; and now add 
sufficient of the urine to fill the bulbous portion of the instrument. 
The saccharimeter and its contents should be set aside at a tem- 
perature of 25° to 35° C. (77° to 95° F.). As a guard against the 
escape of gas, a small amount of mercury may be poured into the 
bent limb of the saccharimeter. Should sugar be present, fer- 
mentation will occur within the course of twelve hours, the carbon 
dioxid formed collecting at the top of the tube, which as a conse- 
quence gradually displaces the urine as the gas accumulates. The 
percentage of sugar present is read from the graduation indicated 
on the perpendicular hmb of the saccharimeter and this is to be 
multiphed by the degree of dilution. 

Corroborative Test. — Introduce a small piece of caustic soda 
into the urine of the tube after the carbon dioxid is collected at 
its upper portion, and it will be seen that, owing to the absorption 
of gas, the Hquid again rises toward the top of the tube. 

Caution. — Yeast in itself may occasionally give rise to the 
formation of a small volume of gas, even in the absence of sugar, 
and it is therefore well to conduct control tests with normal urines. 
Among the other carbohydrates capable of fermentation should 
be mentioned lactose, levulose, and maltose, but should the tests 
with a copper solution prove positive, it is highly probable that 
glucose is present. None of the tests for sugar previously de- 
scribed is capable of demonstrating the minute traces present in 
normal urine, and the reader is referred for this purpose to special 
works upon physiologic chemistry. 

Fehling's Method. — Fehling's solution (see Formula, page 
227) is of such strength that the copper suspended in 10 c.c. will 
be completely reduced by 0.05 gm. of glucose. Urine containing 
sugar should be carefully added to this quantity of the solution 
until the copper is completely reduced, when the amount of sugar 
contained in the specimen of urine may be readily calculated. 
The desired results are most likely to be obtained when from 
5 to 10 c.c. of urine are used in the titration, so that it is neces- 
sary to dilute the urine to the proper degree in the determination 
of this point, the specific gravity serving as a reliable guide (dilute 
five times, urines of specific gravity of 1.030), and to be more certain 
that the degree of dilution is sufficient treat 5 c.c. of FehKng's solu- 
tion with I c.c. of diluted urine, a few drops of caustic-soda solution, 
and enough water to make 25 c.c. Boil the mixture thoroughly, 
and if the liquid still remains blue in color another cubic centi- 
meter of dilute urine may be added and this procedure repeated 
until the two tests differ by i c.c. of urine — the last cubic centi- 



232 THE URINE. 

meter that has been added causing the cuprous oxid to be sepa- 
rated. This precipitate, however, merely determines the ap- 
proximate percentage of sugar present, and is unrehable unless 
all albumin has been previously removed from the urine. 

Testing Fehling's Solution. — Dissolve 0.2375 g^- of crystallized 
cane-sugar, which has been dried at 100° C. (212° F.), in 40 c.c. 
of distilled water, and 22 drops of a one-tenth per cent, solution 
of sulphuric acid. Place the mixture on a water-bath and keep 
at boiling temperature for one hour ; then cool and dilute to 100 
c.c. with distilled water. Every 20 c.c. of this solution contains 
0.05 gm. of glucose, which will reduce the copper in 10 c.c. of 
Fehhng's solution should it be of the required strength. In case 
the solution be too strong, 21 c.c. or more of the sugar solution 
may be required completely to reduce the copper, in which case 
the strength of the Fehhng's solution is determined according 
to the following equation: 

20 : 0.05 :: 2 1 : x, making x = 0.0525. 

Titration. — Place lo c.c. of Fehhng's solution in a beaker and 
to it add 40 c.c. of water. Transfer to a porcelain dish or a flask and 
boil. While this mixture is boiling, add the dilute urine from a buret 
0.5 c.c. at a time (Fig. 90), shaking after each addition, and it will be 
seen that the precipitated cuprous oxid will quickly settle at the bot- 
tom of the dish, forming a white precipitate, while simultaneously 
with this change the blue color of the reagent becomes less and 
less intense as the urine is added until finally the solution is nearly 
colorless. The urine should now be added drop by drop until 
decolorization is complete. Multiply the degree of dilution by 
five, and divide this result by the number of cubic centimeters of 
diluted urine employed. The quotient will indicate the percent- 
age-amount of sugar. 

In case of ordinary diabetic urine dilute i in 20 (5 c.c. of urine 
to 95 c.c. of water), and place a quantity of it in a buret. Place 
10 c.c. of Fehhng's solution in a flask of 100 c.c. capacity, add a 
few drops of caustic-soda solution, 40 c.c. of water, and boil. 
Add the urine from the buret to the boihng fluid until the Hquid 
above the precipitate is decolorized, thus obtaining the approxi- 
mate amount of urine required. Repeat the process in several 
flasks, adding the urine at once in each case until within one-tenth 
of a cubic centimeter of the amount of urine required to decompose 
the 10 c.c. of Fehhng's solution has been found. 

Computation. — Since 10 c.c. of Fehhng's solution equal 0.05 
gm. of glucose, let us suppose 10 c.c. of dilute urine were required 
and 5000 c.c. the product of twenty-four hours' secretion. The 



GLUCOSE. 



233 



sugar 

5000 > 



contained 

0.05 



urine is therefore 



in the twenty-four hours' 
2=; orm.; but since a dilution of i in 20 was em- 

10 JO' 

ployed in the twenty-four hours' urine, it equals 20 X 25 gm., or 
500 gm. 

Difficulties. — It is not at all times easy to determine the exact 
point at which all the copper 
has been reduced (as indicated 
by an entire disappearance of 
the blue color); but when it 
seems likely that this point has 
been reached, it is well to filter 
I c.c. or more of the fluid 
through Swedish filter-paper, 
acidify the filtrate with acetic 
acid, and treat with a few 
drops of potassium ferro- 
cyanid. In the event of any 
copper being present in this 
solution a brown color will be 
formed, which indicates that 
the urine added is not suffi- 
cient; if, however, no brown- 
ing of the liquid results, it is 
probable that the desired point 
has been reached and possibly 
passed. In either case repeat 
the titration for accuracy. 
Again in certain instances the 
precipitate will not collect at 
the bottom of the liquid and 
wiU even pass through the fil- 
ter, thus rendering it impos- 
sible to determine the point of 
end-reaction (accumulation of 
reddish precipitate). 

Cause suggested the follow- 
ing method in such instances: 

Dilute 10 c.c. of Fehling's solution with 20 c.c. of distilled water 
and treat the mixture with 4 c.c. of a one-twentieth of one per cent, 
solution of potassium ferrocyanid. Boil, adding the dilute urine 
drop by drop from a buret until the solution is decolorized. No 
precipitate forms in this method. 

Marshall and Ryan^s Method. — Fehling's solution on a basis 




Fig. 90. — Apparatus for the quantitative estima- 
tion of sugar: tii, Meniscus (Ogden). 



234 



THE URINE. 



of the preparation of looo ex. is made as follows: well-crystal- 
lized, non-effloresced, chemically pure cupric sulphate is pulverized 
and immediately spread on and pressed between sheets of bibulous 
paper to remove any moisture which may have been held mechanic- 
ally by the crystals. Take 34.667 gm. of the pulverized dried 
material, quickly weigh, and dissolve in 400 c.c. of distilled water 
at ordinary temperature, and when complete solution has occurred, 
the Hquid is diluted to 500 c.c. Agitate so that the solution shall 
become homogeneous in its contents of cupric sulphate. Place 
in a rubber-stoppered bottle. 

Approximately 173 gm. of pulverized sodium and potassium 
(Rochelle salts) are dissolved in 480 c.c. of sodium-hydroxid 
solution of 1. 140 specific gravity. After complete solution dilute 
with water to 500 c.c. Keep like the former solution. 

When equal volumes of the cupric-sulphate solution and of the 
Rochelle-salt solution are mixed, FehHng's solution is produced 
and I c.c. of it will correspond to 0.005 gm. of glucose. 

Dilute I c.c. of FehHng's solution with four volumes, of water 
and heat to the boiHng-point to ascertain whether decomposition 
of the solution has occurred. To the solution in the test-tube 
the urine is now added drop by drop from a pipet (noting the 
number of drops used), and after the addition of each drop of 
urine the liquid is heated to about the boiling temperature. Con- 
tinue adding urine until the blue color of the liquid has disappeared. 
As two drops of urine are approximately equal to one-tenth c.c, 
therefore the number of drops of urine employed divided by two 
will furnish a number which, when expressed in tenths, will 
approximately correspond to the volume in tenths of a cubic 
centimeter of the urine employed. 

The following table expresses, in tenths of a cubic centimeter, 
the percentage of glucose present in the urine as indicated by the 
quantity of the urine required exactly to decolorize i c.c. of 
Fehling's solution diluted with 4 c.c. of water: 

Cubic Centimeter Glucose Cubic Centimeter Glucose 

OF Urine. per cent. of Urine. per cent. 

0.1 5-0 04 1-25 

0.12 4.2 0.45 I.I 

0-I4 3-5 0.5 i.o 

0.16 3.1 0.6 0.83 

0.18 2.7 0.7 0.71 

0.2 2.5 0.8 0.62 

0.25 2.0 0.9 0.55 

0.3 1.66 1.0 0,5 

0-35 1-4 

Instead of using the table the following rule may be employed : 
"Divide the whole number 5 by the number of tenths, converted 



GLUCOSE. 235 

into whole numbers, of urine employed. The result will be the 
approximate percentage of glucose." 

Example. — If 12 drops of urine were required for the decoloriza- 
tion of I c.c. of FehUng's solution (two drops approximately 
equaling one-tenth c.c), therefore 12 divided by 2 would 
give 6, which expressed in tenths would represent the number 
of tenths of a cubic centimeter corresponding to the drops of 
urine employed, namely, 0.6. This expressed as a whole number 
and used as a divisor of the number 5 (5 -^ 6) = 0.83 per cent, 
of glucose. 

To avoid computation, note the number of drops of urine 
necessary to decolorize i c.c. of FehHng's solution, and consult 
the following table for the approximate percentage of glucose: 



Drops. 



Glucose Drops Glucose 

PER CENT, UKUi-i,. pj^j^ CENT. 



1 14 0-71 

2 5.0 15 0.66 

3 y?> 16 0.62 

4 2.5 17 0.58 

' 5 2.0 18 0.55 

6 1.66 19 0.52 

7 1.4 20 0.5 

8 1.25 21 0.47 

9 i-i 22 0.45 

10 i.o 23 0.43 

11 0.9 24 0.41 

12 0.83 25 0.4 

13 0.76 

Differential Density Method. — Here, as in all estimations 
for sugar, albumin must be removed by heat and filtration and 
the urine should be sufficiently diluted with distilled water to insure 
that not more than 0.5 to i per cent, of sugar is present. The 
urine must be fresh, as fermentation begins spontaneously when 
the urine is allowed to stand. This method serves as a most 
valuable one in general work and is preferable to many of the 
more uncertain titration methods unless the operator has had 
considerable experience with such methods. Ascertain the spe- 
cific gravity of the urine by means of a pyknometer or hydrom- 
eter, which should be graduated to the fourth decimal, and 
provided with a thermometer graduated to indicate tenths of a 
degree. (Each hydrometer is graduated to read at a certain 
tem^perature.) Take the specific gravity at the temperature 
for which the hydrometer has been constructed, heating or cooling 
the urine as may be found necessary. 

Place 100 c.c. of the urine in a flask and to it add an emulsion 
of fresh live yeast which has been washed free from minerals. The 
flask should be corked loosely in order to allow the escape of gas, 



236 THE URINE. 

and the bottle set aside for from twenty-four to forty-eight hours, 
when again determine the specific gravity, observing the same pre- 
caution previously outhned. Multiply the difference in the spe- 
cific gravity by 230, which factor has been found through estima- 
tions of sugar by titration, polarization, or by the different density 
methods of the urine after fermentation. This result is indicative 
of the percentage of sugar present. Whenever it is desired that this 
process be carried out within a shorter time, add to each 100 c.c. of 
urine 2 gm. of tartrate of potassium and sodium, with 2 gm. of dia- 
cid sodium phosphate and 10 gm. of compressed yeast, keeping the 
mixture at a temperature of from 30° to 40° C. (86° to 104° F.), 
when in a few hours fermentation will be completed. To the 
specific gravity obtained before fermentation should be added 
0.022 to make up for the increase, owing to the addition of the 
salts, that will be observed in the second specimen. 

Optical Saccharimetry. — Grape-sugar exercises a right rota- 
tory power over polarized light, and on this account there is a 
method of both quaHtative and quantitative estimation for sugar 
by the polariscope. If diabetic urine be hght in color, and clear, 
it can be put into the glass tube of the instrument and a deter- 
mination immediately made. 

Caution. — In filhng this glass tube observe that no air-bubbles 
are included with the fluid. But should it be dark and cloudy 
or contain albumin, it is necessary first to clarify the urine and 
remove the albumin and other disturbing substances. 

Clarifying. — Urine may be clarified by adding to ii a 10 per 
cent, aqueous solution of sugar of lead. The lead acetate causes 
a copious precipitate which consists of kad chlorids, phosphates, 
and sulphates, and in addition this precipitate carries down witK 
it nearly all the coloring-matter and albuminous bodies present 
in the urine. The urine is now passed through a dry filter, and 
the filtrate is practically clear and ready for study. It is neces- 
sary to consider the degree of dilution caused through clarifying 
the urine. Take 75 c.c. of urine and to it add 25 c.c. of the lead 
solution; this dilution being observed in our calculation. 

The Saccharimeter. — Elaborately constructed instrumients 
for saccharimetry have been devised by a number of investigators, 
among which that of Ultzmann will be described; and with it 
rapid and fairly satisfactory results in the quantitative estimation 
of sugar may be obtained, should the quantity exceed i per cent., 
but where a smaller percentage of sugar is present, results are 
unrehable. 

Artificial light is not needed, since the instrument is fitted to a 
microscope stand and the illumination accompHshed by the 



GLUCOSE. 



237 



d 



mirror. The tube, objective, and ocular of the microscope are 
removed and in their place the saccharimeter is inserted and held 
in position by a small screw. The concave mirror is then adjusted 
and the instrument manipulated as the microscope (Fig. 91). 
a is a biconcave and h an objective lens of a small telescope, the 
focal distance of which extends to p; c, the upper Nicol prism with 
which the vernier is rather closely connected; ^, a glass tube for 
holding the fluid to be examined; p, the upper 
plate of the right and left rotating quartz ; and /, 
the lower Nicol prism. The arc or fixed scale is 
so divided that each division of it indicates i 
per cent, of grape-sugar when at a temperature 
of 20° C. (68° F.). The vernier enables one to 
estimate tenths of a degree of i per cent., since 
10° C. (50° F.) of the vernier correspond with 9° 
of the arc. To the percentage of sugar found 
should be added as many tenths as there are 
spaces counted on the vernier — up to that divi- 
sion which coincides with a division of the arc. 
Should the zero point of the vernier not quite 
reach (toward the right) the 5 -point of the scale, 
it indicates that the percentage of sugar exceeds 
4 and is less than 5 per cent. When it is desired 
to estimate the tenths per cent, and the sixth 
division of the vernier is the first counted from 
the zero point to coincide with that division of 
the arc, six is the number of tenths required: 
hence the apparatus indicates 4.6 per cent, of 
grape-sugar present. The polarization of cane- 
sugar is three-fourths that of grape-sugar. Both 
cane- and grape-sugar, as well as lactose, possess 
the power to turn the polarized ray to the right — 
albumin and levulose, on the contrary, turn it 
toward the left. 

In case the glass tube of the saccharimeter is 
empty or contains a fluid which holds in solution 
a substance having no optical influence, as has normal urine, the 
zero point of the vernier will be found to coincide with the zero 
point of the scale, and the halves of the field of vision are isochro- 
matic. When an optically active substance is contained in the 
fluid (sugar), this normal isochromatism of the two halves is lost 
and an unequal coloring takes its place, and this inequality of 
coloring depends upon the amount of optically active substance 
contained in the solution. Whenever this unequal coloring is 



/ 



Fig. 91.— Sectional 
view of Ultzmann's 
polarizing sacchari- 
meter. 



238 THE URINE. 

encountered, move the vernier toward the right or left, depend- 
ing upon the substances present (sugar or albumin), until the 
color of the two halves becomes the same, and the percentage is 
then read from the graduated scale. 

Computation. — Suppose to 75 c.c. of highly colored sac- 
charine urine there have been added 25 c.c. of lead solution for 
clarifying purposes, and the filtrate is found by polarimetry to 
contain 4.8 per cent, of sugar. It is necessary to add to this 
percentage 1.6 per cent., since the lead solution added equaled 
one- third the bulk of the urine; therefore 6.4 per cent, equals the 
total amount of sugar present. 

LACTOSE. 

Lactose is to be suspected where a positive reaction is obtained 
with the copper and bismuth tests previously described, and 
negative results are obtained with the phenylhydrazin and fer- 
mentation tests; though it is to be remembered that osazone is 
to be obtained from the pure substances. 

Clinical Significance. — Lactose is commonly found in. the 
urine of nursing women where the flow of milk is impeded and a 
mastitis exists, and it is also encountered in nursing women v^th 
normally well-developed breasts and in wet-nurses. The per- 
centage of lactose may fluctuate between 0.013 ^^^^ 0.438 per 
cent. 

PENTOSES. 

Traces of pentoses — xylose, rhamnose, and arabinose — may be 
found in normal urine. Abnormally large quantities were ob- 
served by Salkowski in a morphin drunkard where pentosuria 
was found to alternate with glucosuria. Bial found two sisters 
and a brother to suffer from pentosuria. Cases have been ob- 
served where digestive pentosuria probably existed. Urines con- 
taining pentoses in rather large amounts reduce Fehling's solu- 
tion and form osazone when treated with phenylhydrazin; but 
the fermentation test is negative. Rhamnose and arabinose pos- 
sess the power of turning the plane of polarized light to the right ;, 
xylose remaining negative (see Optical Saccharimetry, page 236). 

Bail's Test. — Mix one to one and one-half gm. orcin, 500 
gm. of fuming HCl, and 25 to 30 drops of ferric-chlorid solution. 
Place 3 c.c. of the urine in a test-tube and to it add 5 c.c. of the 
reagent. Close the test-tube with a plug of cotton and heat over 
a flame until bubbles begin to form, when a green pigment is 
almost immediately deposited in the presence of pentoses. When 
a small amount is present, the pigment does not become per- 
ceptible until after fifteen to twenty seconds. This reaction is 



BILE IN THE URINE. 239 

claimed to be negative with normal and with diabetic urines. It 
would appear questionable as to whether or not this test will 
differentiate glucosuric compounds from pentoses. 

Tollen*s Phloroglucin Test. — Place several cubic centi- 
meters of phloroglucin in a test-tube, add one-half to one c.c. of 
the urine, and heat, when a deep- red color appears in the presence 
of pentoses. This reaction is also produced by glycuronates. 

Clinical Import. — Maltose, levulose, dextrin, laiose, inosite, 
and animal gum may at times be found in the urine, but their 
clinical significance remains unsettled. While glycuronic acid 
is to be met with in the urine, it is of no known cHnical importance. 



BILE IN THE URINE. 

Bile-pigment and also bile acids are to be met with in the 
urine and usually occur together, in which instance the pigment 
is much more abundant than are the acids. Obstruction of the 
bile-passages serves as a common cause for the entrance of the 
bile and its contents into the urine. It also remains a question 
whether or not traces of bile acids are present in normal urine. 
Biliary urine while fresh contains bilirubin, but after it has stood 
for a time biliverdin is formed as a result of oxidation. To 
the naked eye, urine containing bile is of a greenish or brownish- 
yellow hue, may at times be viscid, and upon shaking displays 
a heavy froth which partakes of the color of the urine. This 
froth serves to distinguish biliary urine from other urines known 
to display excessive froth when agitated; viz., albuminous urine 
(blood, pus, vaginal secretions, etc.), diabetic urine, urine rich in 
urates, calcium oxalate, phosphates, urine after the ingestion 
of salol, and occasionally those containing large amounts of 
other mineral products; but in none of these save urates does 
the froth partake of the color of the urine. 

Tests for Bile. — i. Place a few drops of the urine in a porce- 
lain dish, and at a point one-half to one inch distant from it place 
two or three drops of yellow nitric acid. By means of a glass 
rod draw the urine across the porcelain surface to meet the acid, 
when, upon their union, a display of colors immediately develops. 

2. Place 50 c.c. of urine in a beaker and to it add 5 c.c. of a 
10 per cent, solution of barium chlorid and 5 c.c. of chloroform. 
Shake well, and allow to stand for ten minutes. The precipitate 
which forms will be found to consist of phosphates, bile-pigment, 
and chloroform. Lift a portion of this precipitate in a pipet, 
place it on a shallow dish, and heat over a water-bath until the 
chloroform has evaporated, after which cool and pour off all 



240 THE URINE. 

the fluid from the precipitate. The precipitate is now of a yellow- 
ish hue, and when treated with a drop of impure nitric acid directly 
upon the surface of the dish, the bile-pigment causes a display 
of colors to appear around the drop. This reaction reveals the 
presence of 0.2 per cent, or more of bile. 

3. lodin Test. — Place 10 c.c. of urine in a test-tube and 
allow to flow upon it, entering along the side of the tube, a 10 per 
cent, alcoholic solution of iodin. At the zone of contact of the 
liquids an emerald-green layer appears and is due to the presence 
of bile. 

Test for Bile Acids. — Oliver has proposed a test which 
depends upon the power of the bile acid to precipitate peptone 
when in acid solution. 

Reagent. — 

R , Powdered peptone \ dram 

Salicylic acid 4 grains 

Acetic acid ^ grain 

Distilled water 8 ounces. 

Place 20 minims of clear filtered urine in a test-tube and to it 
add 60 minims of the reagent. In the presence of bile acids a 
decided milkmess at once appears, and should the acids be large 
in amount, this turbidity is most apparent. Agitation often causes 
it to disappear, but it readily reappears on the addition of the 
reagent. This test is exceedingly delicate and thus far is believed 
to be one of the most reHable for the detection of bile acids in the 
urine. 

ACETONE, 

Hydroxybutyric acid, aceto-acetic acid, and acetone are all to 
be met with in the urine, and the relationship existing between 
these three substances is explained by the following formulas : 

Hydroxybutyric acid = CH3CH(OH)CH2COOH. 
Aceto-acetic acid = CH3CO,CH2COOH. 

Acetone = CH3,CO,CH3. 

Hydroxybutyric acid is the first to be formed from the destruc- 
tion of proteids (probably), and after oxidation yields aceto-acetic 
acid, and in turn aceto-acetic acid is readily decomposed into 
acetone and CO2. 

Test for Aceto-acetic Acid. — Fill a test-tube one-third its 
depth with fresh urine, and to it add a few drops of a solution of 
perchlorid of iron (diluted to a pale cherry color) until the pre- 
cipitate of phosphate and iron ceases to fall; filter, and to the 
filtrate add another drop or more of the iron solution. In the 



ACETONE. 241 

presence of aceto-acetic acid a claret color develops which dis- 
appears upon boiling. Salicylates, carbolic acid, antipyrin, and 
similar drugs cause a claret color with perchlorid of iron, and are 
to be differentiated from that produced by aceto-acetic acid by 
the fact that the color induced by these drugs does not disappear 
on boiling. 

Tests for Acetone. — I. (a) Acetone urine emits a fruit- 
like odor. 

(b) Reduces Fehling's solution, and the test which serves most 
readily to identify this substance is to convert it into iodoform. 

II. Place about one inch of urine in a test-tube and to it add 
five drops of a 10 per cent, solution of caustic soda or potash; 
heat gradually and add, drop by drop, a saturated solution of 
iodin in potassium iodid until the liquid assumes a yellowish- brown 
color. Again, add a few drops of caustic- soda solution. A 
yellow turbidity ensues which soon collects at the bottom in the 
form of a crystalKne precipitate emits the odor of iodoform. 
Microscopically this precipitate consists of hexagonal plates which 
are at times in rather dense aggregations and in the form of stars. 

In case there is but a trace of acetone present it will be found 
necessary to distil the urine after the addition of phosphoric 
acid, and then test the distillate as above described. 

Clinical Significance. ^Acetone under normal conditions 
may appear as a mere trace in the urine, at which time the amount 
excreted during the twenty-four hours may vary from 0.008 to 
0.025 gm. 

Diet. — The quantity of acetone excreted is influenced by 
the character of food ingested; e. g., the withdrawal of carbo- 
hydrates causes a decided increase which reaches its maximum 
point in from five to eight days, at which time 100 to even 700 mgm. 
may be excreted daily. Such examples of acetonuria disappear 
where carbohydrates are given with the food. Acetonuria is most 
decided when the diet has contained the minimum amount of albu- 
min and no carbohydrates. It is also marked during starvation. 

Acetonuria is a feature of diabetes, wasting diseases, and of 
both acute and prolonged febrile conditions. 

Diabetes. — The appearance of acetone in the urine of dia- 
betics is of great clinical significance, and when acetone and sugar 
are both present, the amount of the former is in rather direct 
correlation with the severity of the disease. With a gradual daily 
increase in the amount of acetone a fatal issue is to be expected 
at an early date. As previously stated, the addition of carbo- 
hydrates to the food may lessen greatly the daily excretion of 
acetone, and it is questionable whether or not the approach of 
16 



242 THE URINE. 

diabetic coma may be delayed through the administration of 
carbohydrates. 

Fevers. — Here should be mentioned pneumonia, typhoid 
fever, acute articular rheumatism, miliary tuberculosis, septicemia, 
scarlet fever, measles, tonsilHtis; as well as phthisis with cavity 
formation and other intermittent fevers. 

Caution. — In continued fevers the large amount of acetone 
excreted through the urine is dependent in part, at least, upon 
the fact that such patients are not fed Hberally upon carbohy- 
drates and albumins. 

Nervous Diseases. — Acetonuria is also observed in such 
nervous conditions as melancholia, general paresis of the insane, 
major epilepsy, locomotor ataxia; and where malnutrition is in 
evidence. 

Gastric Carcinoma. — An exception to general loss of flesh 
as an accompanying feature of acetonuria is the fact that ace- 
tonuria is hkely to obtain early during the course of gastric car- 
cinoma, and even before emaciation is apparent. 

Chloroform. — Chloroform anesthesia is often followed by 
acetonuria. 

It is generally conceded that acetonuria may result from certain 
gastro-intestinal derangements {enterogenic acetonuria) ; and it 
is probable through this manner that asthma is associated with 
acetonuria. Acetonuria further suggests that there is a general 
breaking down of the circulating albumins. 



OXYBUTYRIC ACID. 

Detection. — Oxybutyric acid is detected, or at least sus- 
pected to be present, in diabetic urine when the urine, after sub- 
jection to fermentation, rotates the plane of polarized hght to 
the left (see Optical Saccharimetry, page 236). 

Caution. — Albumin also exercises a rotatory power and must 
needs be removed by boiling and filtration. Decolorize highly 
colored urines. 

Clinical Significance. — The presence of oxybutyric acid in the 
urine is of special cHnical moment in connection with diabetes mel- 
litus, occurring only in severe forms of this disease. The quantity 
of oxybutyric acid present is usually in direct relation to 
the amount of sugar excreted. Oxybutyric acid is omnipresent in 
the urine of diabetic coma, and is believed to contribute toward 
the auto-intoxication now conceded to be responsible for such coma. 
Stadelmann has suggested that the acid exercises a toxic effect 
by absorbing alkali from the blood. 



DIACETIC ACID. 243 

Oxybutyric acid has been found in the urine during the course 
of acute exanthematous conditions and in scurvy. It may also 
be found during insanity. The relation existing between the 
excretion of oxybutyric acid and of ammonia is of valuable chnical 
importance (see Ammonia, page 246). 



DIACETIC ACID. 

Diacetic acid is not a constituent of normal urine, and when 
found present in this secretion is of practical chnical importance. 
There is, as a rule, a co-appearance of oxybutyric acid, acetone, 
and diacetic acid in the same urine. Diacetic acid is a product 
of the further oxidation of oxybutyric acid (Vierordt), and eventu- 
ally diacetic acid is decomposed into acetone and carbonic acid. 

Gerhardt's Test. — i. Diacetic acid is detected in the urine 
by treating 10 c.c. of the suspected specimen with a solution of 
perchlorid of iron, which should be added drop by drop. The 
addition of the iron solution may cause a precipitate of phosphates, 
which sediment is removed by filtration. Treat the filtrate 
further with the iron solution, and should diacetic acid be present, 
a Burgundy-red color develops, which may deepen to a dark- 
brown. 

2. Boil a second quantity of the urine and treat as in the case 
of No. I. In the event of no reaction taking place, proceed as 
follows : 

3. Place 10 c.c. of the urine in a test-tube; add a small quan- 
tity of sulphuric acid, and extract with ether. Treat this ethereal 
extract with the perchlorid of iron solution as outHned above, 
when the red color will develop. Upon standing for twenty-four 
hours the red color will be seen to fade, and eventually to disappear, 
should such color be due to the presence of diacetic acid, "if 
acetone is present at the same time" (von Jaksch). 

Arnold^s Test. — Reagents. — (a) A solution of paramido-aceto- 
phenone: dissolve one gm. of paramido-acetophenone in 100 c.c. 
of distilled water. Add to the solution hydrochloric acid, one 
drop at a time, until the yellow color disappears, care being 
taken that no more hydrochloric acid be added than is absolutely 
necessary to cause a colorless solution, (b) A solution of sodium 
nitrile (i per cent.). 

Method. — I. At the time of use place 6 c.c. of solution (a) 
in a test-tube, and to it add 3 c.c. of solution (b). 

2. Add an equal volume of filtered urine (filter highly colored 
urine through animal charcoal), and follow with a few drops of 
ammonia. 



244 THE URINE. 

3. With this solution, normal urine will be found to show a 
variable degree of color, which becomes brown or brownish red 
after the mixture is thoroughly shaken. In the presence of 
diacetic acid a reddish-brown amorphous precipitate collects at 
the bottom of the fluid after the tube has been allowed to stand 
for a short time. 

4. Place I c.c. of the supernatant colored liquid in a dish, and 
to it add 10 c.c. of concentrated hydrochloric acid. Diacetic acid 
when present in appreciable amount causes a purpHsh- violet color. 

It is claimed for Arnold's test that it does not react with acetone, 
oxybutyric acid, bilirubin, and after the administration of anti- 
pyretics, saHcylic acid, etc. 

Clinical Significance. — Diacetic acid may be found in the 
urine in diabetes mellitus, where it may exist for a long period 
of time without coma, and during the course of the acute fevers, 
including typhoid, scarlet fever, pneumonia, articular rheu- 
matism, tonsillitis, etc. Diaceturia may also occur during febrile 
conditions of an intermittent type. Again, diacetic acid is a not 
infrequent constituent of the urine of fevers in children, and is 
to be found in the urine during the course of gastro-intestinal 
derangements. 

Diacetic acid is commonly present in conjunction with acetone, 
and is always of serious moment when found in the urine of 
adults. ''If diaceturia is present, oxybutyric acid is also present 
in the urine" (Vierordt). Von Jaksch has suggested that the con- 
vulsions occurring during acute febrile diseases in children are 
accompanied by diaceturia. 

LACTIC ACID. 

Lactic acid (or sarcolactic, as it sometimes occurs) is not a 
constituent of normal urine, but it may rarely be observed during 
disease. 

Reagents. — {a) Alcohol 95 per cent. 

(h) A dilute solution of sulphuric acid. 

(c) Sulphuric ether. 

{d) A I per cent, solution of basic acetate of lead. 

{e) Zinc carbonate. 

Method. — I. Place a few cubic centimeters of the suspected 
urine in a dish, and evaporate over a water-bath to a syrupy con- 
sistence; then extract with 95 per cent, alcohol. 

2. At the end of twenty- four hours remove the supernatant 
alcohol, and again evaporate the mixture to a consistence of syrup ; 
after which acidulate with a weak solution of sulphuric acid. 



CHOLESTERIN. 



245 



3. The mixture is now extracted with ether, continuing the 
process as long as the mixture displays an acid reaction. 

4. Remove the ether by distillation, and dissolve the residue 
in a small quantity of water. 

5. Place the watery mixture in a test-tube, and to it add, drop 
by drop, a small quantity of the lead solution. The mixture is 
now filtered, and the lead that is yet remaining removed with 
sulphureted hydrogen. 

6. Place the filtrate in a dish, and evaporate to dryness over 
a water-bath, the faintly yellowish, sticky residue being lactic 
acid. 

7. Dissolve the residue in a small quantity of water, and heat 
the mixture with zinc carbonate until it is saturated, when upon 
evaporation zinc lactate will be found to separate in the form of 
small crystalline prisms. 

Clinical Significance. — Sarcolactic acid is a constituent of 
the urine in certain hepatic maladies. 



CHOLESTERIN. 

Crystals of cholesterin (Fig. 92) are rarely met with in urinary 
sediments. Von Jaksch detected cholesterin in tabes dorsahs and 





Fig. 92.— Cholesterin crystals (Ogden). 



in cystitis; Simon found it in acute nephritis, and I have en- 
countered it upon three occasions — two of the urines were re- 
covered from cases of chronic cystitis, and in the third an echino- 
coccic cyst had ruptured into the urinary tract. The fresh urine 
containing cholesterin displays an acid reaction, is usually turbid, 
and when shaken vigorously, numerous white, flaky scales are 
to be seen throughout the liquid. Cholesterin is commonly 
found in the fluid recovered from cysts and in feces (see Tests 
jor, page 370). 



246 THE URINE. 

AMMONIA IN THE URINE. 

Ammonia is a constituent of normal urine, from 0.05 to 
0.08 gm. being excreted daily. The quantity of ammonia will 
be found greatly increased when the urine contains oxybutyric 
acid, such increase bearing a direct relation to the amount of oxy- 
butyric acid present. During the course of diabetes mellitus it is 
common to find from 2 to 6 gm. of ammonia excreted during 
the twenty-four hours, and such patients are in imminent 
danger of developing diabetic coma. At this time the urine is 
usually rich in acetone, oxybutyric acid, and diacetic acid. (See 
Urea, page 192.) 

CYSTIN. 

Cystin is occasionally found to form one of the deposits of 
acid urine, and its recognition depends upon the microscopic 
characteristics of its crystals. Cystin precipitates disappear from 
alkahne urines since they are soluble in alkahs, but such 
urines are hkely to putrefy and give off an odor of sulphureted 
hydrogen. 

Tests. — Place 10 c.c. of urine in a test-tube and to it add i 
c.c. of a 30 per cent, solution of caustic potash. Boil, and while 
boihng add, drop by drop, a solution of acetate of lead (2 to 10 
per cent.). A black precipitate of lead sulphid develops. 

Clinical Significance. — Cystin is far more common in the 
urine of males than in that of females, and it is rarely to be met 
with in the aged. Several cases have been reported as occurring in 
members of the same family. Cystinuria may be persistent or inter- 
mittent. It occurs in the urine where there exists a cystin cal- 
culus. 

PYURIA. 

Urines containing pus usually display a rather heavy whitish 
or creamy precipitate which forms as a soHd sheet at the bottom 
of the liquid, and when the bottle is shaken, the sediment becomes 
ropy or shred-hke. Pus may occur in the urine in conjunction 
with blood or with hemoglobin, in which case the naked- eye 
appearance of the precipitate (dark) is somewhat misleading. 
Urines containing pus are likely to be rich in albumin, and a point 
of special interest is to determine whether or not all the albumin 
present results from the pus, or whether true renal albuminuria 
exists. Reinecke suggested the collecting of the twenty-four 
hours' urine, shaking it thoroughly and then estimating the number 
of pus-cells by the hemocytometer. He believes that 100,000 pus- 



ALKAPTONURIA. 247 

cells per c.mm. should correspond to i per cent, of albumin, as shown 
by Esbach's albuminometer. Taking into consideration the many 
factors that may interfere seriously with the dilution of the urine 
and consequently render our count valueless, this procedure seems 
hardly worthy of recommendation. It is probably far better 
to endeavor to ehminate albumin originating along the urinary 
tract by filtration, since renal albumin is thus separated from the 
urine with great difficulty. 

Tests for Pus. — Urines which contain pus develop a green 
color on the addition of a solution of guaiac, which disappears when 
the mixture is heated. Add hquor potassium to the deposit of pus 
and the sediment becomes ropy and later forms into a gelatinous 
mass. The best evidence of pus in the urine is the detection of 
pus- corpuscles (cells) by the microscope. 

Clinical Significance. — The urine may contain pus whenever 
there is a suppurative process either involving any portion of the 
genito-urinary tract, or where pus may escape into the tract 
through a fistulous opening. Pus may also have its origin in the 
vagina or cervix, and true pyuria should be distinguished 
from this condition, which simulates pyuria of urinary ori- 
gin closely, by catheterization of the patient. 



ALKAPTONURIA. 

Alkaptonuria is a condition wherein the urine presents the 
natural color when voided, but after exposure to the air and light, 
it becomes gradually dark on the surface, which darkening ex- 
tends toward the bottom of the liquid and eventually becomes a 
reddish brown, dark brown, or black. This color is dependent 
upon the presence in such urines of dihydroxyphenylacetic acid. 
Melanin and also phenol or its derivatives, when present in the 
urine, cause it to become dark after exposure. 

When alkapton is treated with a small amount of alkah, the 
color appears much earher, and in fact almost immediately; 
and upon application of heat Fehling's solution is reduced by such 
urines. It is to be distinguished from glucosuria, however, by the 
fact that negative results are obtained with the bismuth test (page 
229). With an ammoniacal silver solution reduction occurs 
without heat; and a bluish-green color develops (temporarily) 
when the urine is treated with a ferric salt. The fermentation 
test, phenylhydrazin test, and polarimetry are also negative. 

Garrod's Test. — Heat loo c.c. of the fresh urine to near the 
boihng-point and add 5 or 6 gm. of soHd neutral lead acetate. 
Upon dissolution of the lead a bulky grayish precipitate forms, 



248 THE URINE. 

which is removed by filtration. The filtrate (pale yellow) should 
be set in a cool room for twenty-four hours. Should the urine 
be rich in homogentisinic acid, minute, acicular, almost colorless 
crystals begin to form after several hours, and in case the flask 
containing the urine be set upon ice, crystallization is hastened. 
These crystals are grouped to form rosets and stars and are 
rather deeply colored. Should crystallization be tardy, again 
heat the urine and add more of the lead acetate. The crystaUine 
product thus obtained is lead homogentisinate, and is soluble in 
hot water, but upon its solution the hquid becomes a deep brown 
when an alkaU has been added. It reduces FehHng's solution 
and causes a deep-blue color with a dilute solution of ferric chlorid. 

Clinical Significance. — Alkapton may appear spontaneously 
in the urine of apparently healthy individuals. Garrod* states, 
that the condition is to be met with in several members of a family, 
and cites cases demonstrating this point. It affects brothers and 
sisters ahke, but has not been shown to be transmissible from 
one generation to another. Intermarriage exercises some influence 
favoring the development of this condition, and older members of 
the family are less Hable than are the younger ones. Pavy has 
observed a family in which the parents were first cousins, where 
four of fourteen children were alkaptonuric. Mittlebach | reports 
an interesting case in conjunction with a chemic analysis of the 
substance. The amount of homogentisinic acid ehminated in 
twenty-four hours is variable and may reach 4.6 gm. An in- 
creased excretion follows the excessive ingestion of meats. 



UREIN. 

Moor,f of Rome, Italy, claims to have discovered a substance 
in the urine which is probably one of the most valuable contri- 
butions to recent urinology should it stand the test of criticism. 
Urein is described as being an oily Hquid, of heavy specific gravity,, 
and of a pale yellow color, resembling olive oil. Weatherson § 
has contributed a valuable monograph upon the chemistry of 
this substance. In 50 c.c. of urine nearly two ounces of liquid 
urein are claimed to exist, though the latter observer was unable to 
recover this quantity from the twenty-four hours' product. Urein 
remains intact and constant at a temperature below 75° to 80° 
C. (167° to 176° F.), yet further thorough and careful investiga- 
tion needs to be made by other observers. 

* " Lancet," Nov. 30, 1901. f "Deut. Archiv f. klin. Med.," vol. Ixxi, pt. L 
X " Proc. Inter. Med. Con.," Paris, 1900. 
§ "Jour, Amer. Med. Ass.," March 16, 1901, p. 723. 



ehrlich's dimethylamidobenzaldehyd reaction. 249 

EHRLICH DIAZO-REACTION. 

Under certain pathologic conditions associated with high 
fever a chromogen is to be found present in the urine, which, when 
treated with diazobenzinsulphonic acid in the presence of am- 
monia, causes a distinct red color which may vary from a rose- 
pink to a garnet. The reaction probably depends upon the fact 
that if sulphanilic acid (amidosulphobenzol) be acted upon by 
nitrous acid, diazosulphobenzol results, and unites with the 
aromatic compounds present in the urine, forming an anilin color. 

Reagents. — i. A solution of sulphanilic acid (i gm. to every 
100 c.c.) in 5 per cent, hydrochloric acid. 

2. Solution of sodium nitrite one-half per cent. It is neces- 
sary that both solutions be fresh. 

Method. — Place 10 to 20 c.c. of urine in a test-tube and to 
it add an equal volume of solution No. i, shaking gently to effect 
a perfect mixture; then add from three to six drops of solution 
No. 2, and shake until a heavy froth collects. Render alkahne 
with ammonia. The diazo-reaction consists in the Hquid becom- 
ing a port- wine color while the froth is also red. 

Clinical Significance. — The diazo-reaction is a fairly con- 
stant symptom of typhoid fever after the second week of the 
disease. I have found it present repeatedly in cases of measles, 
tuberculosis (with cavity), meningitis, croupous pneumonia, in 
a number of rather obscure conditions, the majority of which 
were associated with high fever; and less often in scarlet fever, 
acute miUary tuberculosis, erysipelas, pyemia, diphtheria, puer- 
peral sepsis, and tonsilHtis. It has not, therefore, proved to be of 
great diagnostic value in typhoid fever, since the disease is usually 
capable of diagnosis before the urine displays this reaction, though 
certain of its advocates claim that the reaction is to be found 
as early as the fifth day of the disease. In pulmonary tuber- 
culosis where the diazo-reaction is present for a long period the 
disease usually progresses with great rapidity. 

EHRLICH^S DIMETHYLAMIDOBENZALDEHYD REACTION. 

It remained for EhrHch * to point out that under certain con- 
ditions dimethylamidobenzaldehyd induced a red color with 
mucus of some pathologic urines (which are always of high speci- 
fic gravity — 1.026 to 1.034), and that a reaction resembhng this, 
though less intense, was also given with normal urines. Patho- 
logic urines giving this reaction are also Hkely to give positive 
diazo- and indican reactions. Proscher's analytic results are: 

* " Med. Woch.," 1901, No. 15. 



250 THE URIXE. 

carbon 56.49; hydrogen 7.06, and nitrogen 8.28 per cent., and he 
gives the formula C_H^-X for this unknown body. 

Method. — Reagent. — Place 2 per cent, of dimethylamido- 
benzaldehyd in equal parts of concentrated hydrochloric acid 
and water. Place 10 to 20 c.c. of the urine in a test-tube, and to 
it add from five to ten drops of the reagent; agitate to effect a 
mixture and set aside for a few minutes (two to four) and then 
note the color. The reaction is positive when a cherry-red color 
develops and takes place with certain pathologic urines. Normal 
urines may show a deepening of their normal color, redden sHghtly, 
or change to a greenish yellow. Even with pathologic urines the 
intensity of the red color is variable. It may develop upon contact 
of the first drop of the reagent with the urine; or it may require 
several drops of the reagent, and two to four minutes' exposure 
before the maximum intensity is attained. The pigment can be 
extracted in part with chloroform. 

Caution. — After standing for five minutes the cherry-red color 
is apt to give way to a dark amber, yet rarely, with a decided 
reaction, the color may persist for hours and even days. 

Clinical Significance. — Positive results may be obtained 
wdth the urine of tuberculosis in 40 per cent, of cases. The cHnical 
reports of Clemens,^ Koziczkowsky,t and Simon 1 show that the 
reaction is also common to the urine of both febrile and non- 
febrile maladies, among which are to be mentioned gastro- enteritis, 
alcoholism, appendicitis, chronic plumbism, gastric carcinoma, 
esophageal carcinoma, lobar pneumonia, bronchitis, subphrenic 
abscess, facial erysipelas, measles, and typhoid fever. 

THE VOLATILE FATTY ACIDS. 

Volatile fatty acids when present in the urine are usually 
described under the caption of lipaciduria, although the term, more 
correctly speaking, implies an increased elimination of this sub- 
stance. The fatty acids which have been found in the urine are 
acetic, butyric, propionic, and formic acids. 

Detection. — i. The detection of fatty acids in the urine is 
accompHshed by distilling the urine with phosphoric acid; the 
distillate cautiously neutralized with carbonate of soda, and 
evaporated to dryness over a water-bath. 

2. Extract the residue '^^ith hot alcohol; filter, and again 
evaporate to dr}'ness over a water-bath. 

* " Deut. Arch.," igoi, vol. Ixxxi, p. i68. 

t " Berl. med. Woch.," IQ02, vol. xxxix, Xo. 44. 

X " Amer. Jour. Med. Sci.," Sept., 1903, p. 471. 



FAT. 251 

3. Dissolve this second residue in water, and to this liquid 
apply a small quantity of a solution of perchlorid of iron (the 
solution of formic acid must be neutral in reaction), when a blood- 
red color develops. Heat this solution gradually to the boiling- 
point, when the color, should it be due to formic acid, fades and 
eventually disappears, leaving the deposit of a rusty colored 
sediment at the bottom of the liquid (see Feces). 

Place 10 c.c. of the urine in a test-tube, and to it add one- 
fourth this volume of sulphuric acid and alcohol, when, in the 
presence of acetic acid, an odor of acetic ether is emitted. 

It is important to note that free formic acid is not precipitated 
by nitrate of silver; but that the alkaline salts of formic acid are 
precipitated from concentrated solutions containing this sub- 
stance by nitrate of silver; a white precipitate results which soon 
changes to a black should formic acid be present. 

Microscopically, volatile fatty acids may appear in the form 
of needle-hke crystals (see Feces). 

Clinical Significance. — Normal urine contains traces of the 
fatty acids. Fatty acids are known to occur in excessive amount 
in the urine during the course of leukemia, diabetes, cirrhosis of 
the liver, and in suppurative conditions, among which should be 
mentioned those affecting the serous sacs, e. g., purulent peritoni- 
tis, pleurisy, etc.; and in such acute inflammatory maladies as 
erysipelas and phlegmonous inflammations. 

It is difficult to estimate the true clinical significance of fatty 
acids when found in the urine, and while it is generally conceded 
that the degree of carbohydrate fermentation present in the intes- 
tine bears a more or less direct correlation to the amount of fatty 
acids excreted through the urine, further evidence is needed to 
substantiate this behef. 

FAT. 

Fat is not a constituent of normal urine, but during the course 
of certain maladies it may appear in this secretion in rather large 
quantities. This condition is known as lipuria. 

The appearance of sufficient fat in the urine to render it of a 
suspicious appearance is unusual, although there are vaHd records 
of such instances, where the urine has been found to contain fats 
during the course of what otherwise appeared to be normal preg- 
nancy. It is all-important to exclude the possibility of the urine 
being contaminated with fat from structures adjacent to the 
urinary tract. Microscopically it is not unusual to detect small 
particles of fat in the urine. 

Clinical Significance.— Small fat-globules are to be observed 



252 THE URINE. 

microscopically whenever there exists advanced degeneration 
of the renal epithehum. Areas of fatty degeneration are to be 
recognized in such epithelial cells and in the pus-corpuscles. 
Under such conditions droplets of fat may be found free in the 
urine, but it is far the more common to find them intimately 
connected with, or apparently occupying, a portion of some of the 
formed elements (see Fatty Casts, page 289). Lipuria may be pre- 
ceded by Hpemia (see Fat in the Blood, page 66). 

Certain observers have found varying amounts of fat in the 
urine after the administration of large quantities of cod-Hver oil. 
Lipuria is a feature of obesity, pulmonary tuberculosis (stage of 
cavity), leukemia, disease of the pancreas, myocarditis, diabetes 
mellitus, chronic nephritis with fatty kidney, phosphorus-poison- 
ing, pyonephrosis, puerperal eclampsia, chronic alcoholism, and 
conditions in which abscesses and cysts empty into the urinary 
tract. It has been observed to follow multiple fractures of the 
long bones, and in septicemia. 

Staining. — Place a small amount of the urinary sediment 
upon the center of a shde, spread thinly, and dry in the air. Stain 
for one minute with an alcohoHc solution of Sudan III. Re- 
move the stain by allowing a current of water to flow upon one 
end of the sHde and to flood gently over the specimen. AIL 
particles of fat will stain pink or red with this solution. It is 
ofttimes more practical to place a drop of the Sudan III solution 
at the margin of the cover-glass, and to move the cover slightly 
toward the stain; when the red solution will be found to flow 
beneath the cover, mingling with the cellular elements and debris 
present. Thus treated, particles of fat stain a light pink shade. 

For a description of Cammidge's reaction for glycerin in the 
urine see p. 531. 

CHYLURIA. 

Chyluria is the name appHed to a condition wherein the urine 
presents the macroscopic appearance of milk. Chylous urine 
is Hkely to contain albumin, and always contains fat. Upon 
standing, such urine may display a heavy sediment, a portion of 
which sinks to the bottom, while a certain amount of the fat may 
collect upon the surface of the urine, resembhng the cream dis- 
played by milk that has been kept at a low temperature. Further, 
chylous urine may, upon standing, show a tendency toward the 
formation of rather tough coagulum. A portion, and at times 
nearly all, of the urine becomes gelatinized. Chylous urine often 
has a bloody color. 

Recognition. — Place 10 c.c. of the milky urine in a test-tube, 
and to it add an equal volume of sulphuric ether; then shake 
vigorously for several minutes; and set aside for a short time,. 



CHYLURIA. 253 

when the particles of fat are seen to be separated by the 
ether. 

Chemically, fats form a rather constant constituent, and are 
to be recognized through both their chemic and microchemic 
reactions. Albumin also forms a common constituent of chylous 
urine, and is not infrequently present where there exists no other 
evidence of disease of the renal parenchyma. Such albumin 
may result in part at least from the blood that is present in chylous 
urine, but in the absence of blood and other evidence of renal dis- 
ease it is often found present, in which instance its significance 
and derivation remain moot. 

Microscopic. — The sediment of chylous urine is best col- 
lected through the aid of the centrifuge. Such sediment will be 
found to contain for the most part innumerable small refractile 
globules of fat (Fig. 93), epithelial 
cells, few leukocytes, and a variable 
number of red blood-cells, which in 
bloody urine may exceed in number 
the fat-globules. Crystals of leucin 
and tyrosin are occasional findings, 
while cholesterin is rather commonly 
seen. 

Renal epithelium and renal casts 
are to be seen whenever there exists 
nephritis. It is not uncommon to 
find the Filaria sanguinis hominis 

, , . , . . Fig, 93. — Chyle and starch in 

present m chylous Urme a condition mine. Small cells chyle, large and 

1 • 1 T 1 T_ J j^ irregular bodies are starch (obi. 

which i have observed upon two spencer one-sixth). 

occasions. The filaria v^hen passed 

with the urine is non-motile, but in fresh specimens the parasite 

does not appear to be materially distorted. 

Clinical Significance. — Parasitic chyluria is a symptom of 
filariasis, but by no means do all cases of filariasis show chyluria. 
In many instances of chyluria the true cause of this symptom 
is unknown; yet when chyluria is considered with reference to 
the relation of the lymphatics surrounding the kidney, it appears 
reasonable that any condition capable of forming a fistulous com- 
munication between the lymphatics and the pelvis of the kidney 
might excite chyluria. In one instance under personal obser- 
vation chyluria followed an operation for a floating kidney; and 
in another a temporary chyluria developed following a severe fall, 
but this symptom (chyluria) was of but two days' duration. In 
a third case, recently studied, chyluria developed during the course 
of a sloughing uterine fibroid, but the urine became clear three days 




254 THE URINE. 

later and there has been no return of this symptom. It is of 
further chnical interest to note that this patient developed phleg- 
masia alba dolens two months after the attack of chyluria. 

PTOMAINS. 

Despite the vast amount of literature that has recently ac- 
cumulated with reference to the detection of ptomains in the urine> 
we are thus far practically without chnical data that may be re- 
garded of diagnostic value concerning such substances. 

Cadaverin and putrescin have been found in the urine in 
considerable amounts. These substances are to be obtained 
from the cadaver during the process of putrefaction. They 
appear in the rice-water stools of Asiatic cholera and in cultures 
of the comma bacillus, of Koch. Cadaverin is often found in con- 
junction with cystinuria, and according to Simon, the amount of 
diamins found in this condition may vary greatly, he having 
isolated as much as 1.6 gm. of benzoylated cadaverin from the 
twenty-four hours' product. 

GASES, 

Normal urine contains a small volume of gases, which accord- 
ing to Purdy are: carbonic acid 4 to 9 volumes free gas, 2 to 5 
combined; oxygen, 0.2 to 0.6 volume; and nitrogen, 0.7 to o.& 
volume. 

Sulphureted Hydrogen. — Under certain pathologic con- 
ditions sulphureted hydrogen is found in the urine — a condition 
known by the term hydrothionuria. Hydrothionuria may be 
due to the escape of gas into the bladder from the adjacent tissues 
or viscera. In certain instances it has been found to be due to an 
accumulation of pus; and where abscesses have emptied their 
contents directly into the bladder. Again, sulphureted hydrogen 
is a product of the putrefaction of albuminous substances, in which 
case the gas is, at times, due to the development of bacteria. In 
order to prove this point, add a small quantity of the contaminated 
urine to several times its own volume of normal urine; mix thor- 
oughly, place in a sterile test-tube, cork with cotton, and allow to 
stand for twenty-four hours at a temperature near that of the 
body. Should the gas be due to bacterial development, the normal 
urine in the test-tube will contain sulphureted hydrogen; but 
should the sulphureted hydrogen have gained entrance to the 
bladder from without, the urine will be found free from this gas. 

It is not definitely knovm through the development of what 
organism or organisms sulphureted hydrogen is generated in 
the urine, and there is reason to suspect at least that it results from 



EFFECT OF DRUGS UPON THE URINE. 255 

the action of certain bacteria upon some special substance or 
substances present in the urine. In addition to the above sources 
of sulphureted hydrogen in hydrothionuria, it is thought that the 
gas may be derived from neutral and oxidized sulphurs present. 
From the foregoing statements it will be seen that the entire 
question remains unsettled. Hydrothionuria is often associated 
v^ith cystinuria. 

Test for Sulphureted Hydrogen. — i. Place from lo to 30 
c.c. of the suspected urine in a clean bottle. 

2. Cut several strips of filter-paper, about one-fourth inch 
wide by one inch long, and moisten these papers with a solution 
of sodium hydrate, and then with a solution of lead acetate. 

3. Surround the moistened strips of filter-paper by a thread, 
and then lower them into the bottle, clamping the thread with 
the cork, so that the filter-paper will be suspended some distance 
above the urine, and near the top of the bottle. 

Should sulphureted hydrogen be present, the filter-paper will 
be changed to a gray, brown, or black color. The intensity of the 
color and the time necessary for its production will depend upon 
the quantity of sulphureted hydrogen present. 

EFFECT OF DRUGS UPON THE URINE. 

It is the rule for cHnicians to submit specimens of urine for 
analysis without informing the laboratory worker as to the nature of 
the case in question, and much less to think of acquainting him 
with what drugs have been administered to the patient during the 
past few days. Certain medicines are readily detected in the urine, 
while others are detected with great difficulty, and still a third 
class are not demonstrable except when administered in large 
doses, and even then there may be room for question as to their 
identity. It shall be my purpose here to call attention to a few 
drugs which when administered by the mouth produce decided 
changes in the urine. 

Clinical Significance. — The recognition of certain drugs in 
the urine is by no means a feature of great cHnical value, since drugs 
when given as medicinal, and even in toxic, doses are often elim- 
inated with the urine in such small amounts as to make their 
detection impossible or at least impracticable. 

iodin. — Place 5 c.c. of urine in a test-tube and to it add from 
two to five drops of fuming nitric acid. Add chloroform to equal 
the quantity of urine, shake gently, and set aside for a few minutes. 
Chloroform will be found to settle at the bottom of the tube and 
display a reddish-violet color. 



256 THE URINE. 

Bromin. — Bromin when present in the urine may be detected 
in the same method as is iodin, differing only in that bromin 
colors the chloroform a brownish yellow. 

Potassium iodid gives a pink color to the chloroform when 
treated as in testing for indican (page 211). 

Salicylic Acid and the Salicylates. — Following the adminis- 
tration of saHcylic acid, the urine will be found to strike a 
blue- violet color when treated with a solution of chlorid of iron 
(see Diacetic Acid, page 243). 

Salol. — Urine containing salol becomes green, and eventu- 
ally black, upon staining (see Color, page 169). It gives the re- 
actions for saHcylic acid. 

Antifebrin. — This substance may be detected in the urine 
by the following method: Place a few cubic centimeters of 
the fresh urine in a test-tube and to it add one-fourth this 
volume of a concentrated solution of hydrochloric acid; boil 
gently for from one to three minutes, and set aside until cool. 
To the cold mixture add a few cubic centimeters of a weak solu- 
tion of carboHc acid (3 per cent.), and follow by adding, a drop 
at a time, a weak solution of chromic acid. The entire mixture 
assumes a red color; but upon being alkahnized by the addition 
of ammonia it changes to a blue. Antipyrin also causes a red 
color when treated with a solution of chlorid of iron ; and thallin 
causes a greenish-brown color with this reagent. 

Rhubarb and Senna. — Rhubarb and senna are known to 
give a decided color to the urine. These substances have been 
described under Color, page 169. 

Carbolic Acid. — Following the administration of carbolic acid, 
resorcin, and naphthahn, the urine will be found to contain 
hydroquinon in considerable amounts ; and upon standing exposed 
to the light, such urines darken, becoming first olive-green, and 
later brownish black, or in some instances black. The exact 
determination as to which of these drugs has been administered 
is of no practical value except in the case of poisoning (see special 
works on toxicology). 

Poisons. — Whenever arsenic, antimony, lead, mercury, and 
silver have been administered in sufficient quantities to produce 
poisonous effects, these metals will be found to appear in the urine. 
They are also found after the prolonged use of these drugs in 
medicinal doses. The amount of the metal excreted through 
the urine is comparatively small, and it is questionable whether 
its detection in this secretion is of practical cHnical value except 
it be studied from a toxicologic standpoint. 

Among the alkaloids, quinin and strychnin are often excreted 



MICROSCOPIC STUDY OF THE URINE. 257 

through the urine unaltered, yet here, too, the amount is extremely 
small. Morphin may be excreted through the urine, but this is 
not a constant finding following the administration of this drug. 
It is scarcely \^'ithin the scope of this volume to deal further with 
the question of drugs, and the reader is therefore referred to special 
works upon toxicology. 



MICROSCOPIC STUDY OF THE URINE. 

Normal urine is acid, and when allowed to stand for a few 
hours deposits a cloud of variable density at or near the bottom 
of the vessel, which deposit is sometimes prevented from forming 
by the rapid development of fungi. This sediment is composed 
of crystals, epithehal cells, mucus, white blood-cells, and granular 
debris. Urine voided in the morning is apt to deposit urates, 
and may at times show uric acid and calcium-oxalate crystals. 

Pathologic urines may be alkahne or acid, and are often cloudy 
when voided, or deposit a heavy sediment on standing; yet it 
does not necessarily follow that all morbid urines display a pre- 
cipitate ; on the contrary, the urine of chronic interstitial nephritis 
is exceptionally free from sediment, as is also diabetic urine. 

Microscopic study of the sediment from pathologic urine that 
has not undergone decomposition outside the body always fur- 
nishes valuable clinical knowledge and frequently provides the 
only rehable information on which to base a diagnosis. 

SEDIMENTATION. 

Two methods are employed in effecting a precipitate of the 
organic and inorganic constituents of the urine: i. Allow the 
urine to stand in a cool place until sufficient sediment has col- 
lected at the bottom of the Hquid. 2. By means of the centri- 
fuge (Fig. 75); which instrument should be so constructed as 
to make it impossible for the tubes containing the urine to come 
in contact with its handle, a defect in many American patterns. 

In using this instrument let steadiness, rather than rate of 
speed, receive first attention. Such instruments propelled by 
water and by electricity are in use, and I have found them most 
satisfactory. Shake the urine well and then pour it into the centri- 
fuge tube to within one-fourth of an inch of the brim; place the tube 
in its special receptacle on the armature {seeCentrijuge, page 189) 
and in the opposite receptacle place a tube filled with urine, 
or with water to balance the instrument. Centrifugate for from 
three to five minutes, when a precipitate will have collected at the 
17 



258 THE URINE. 

bottom of the tubes. Remove the tubes from the armature and 
stand them in an ordinary tumbler. 

Caution. — The tubes are marked by a small elastic which sur- 
rounds the top of one tube. 

MICROSCOPIC TECHNIC. 

The precipitate is hfted by means of a pipet and a small drop 
of it placed on the center of a shde, which is placed on the mic- 
roscope, and the specimen viewed under a low-power objective 
(two-thirds) to determine its general character. Certain organic 
and inorganic elements, as phosphates, urates of ammonia, 
uric acid, epitheha, and casts, are determined through this ob- 
jective, and fungi may be recognized with a variable degree of 
certainty. 

Light. — In the study of urine a small amount of hght is 
required, since a high degree of illumination prevents seeing many 
objects of diagnostic value, high hght rendering translucent 
bodies transparent; thus fatty acids, phosphates, tyrosin, soaps 
of calcium and magnesium, and other deUcate crystals, as well 
as hyahne casts and epitheha, often escape notice when the hght 
is not properly adjusted. To avoid such an error it is my practice 
to employ an Abbe condenser and an iris diaphragm in the study 
of all urines. A second diaphragm above the substage is of 
Httle value. 

The hght may also be advantageously modified by interposing 
colored plate glass or gelatin paper between the mirror and 
condenser. A complemental color to the stain gives best results; 
e. g., for methylene-blue use red or yellow; for safranin employ 
green. 

After a specimen has been studied under a low power the 
slide is removed from the microscope, placed on the table, and 
a clean cover- glass allowed to fall gently upon it. It may now 
be studied through a higher power objective. For general urinary 
work a one-fifth or a one-sixth objective is of most service. 

Focus. — These objectives focus at a point just sufficiently dis- 
tant from the cover-glass to permit the eye to carry between the 
tip of the objectives and the cover, the head having been lowered to 
bring the eye on a level with the microscope's table (page 22). 

Permanent Mounts. — It is difficuk, if not impossible, to 
acquire sufficient knowledge of the various crystals and their many 
forms found in urinary sediments, as well as the rare organic sub- 
stances encountered, to enable one to make a positive assertion as 
to the nature of any crystal or cell which he may meet in general 



MICROSCOPIC TECHNIC. 259 

urinary microscopy; and to insure against all possible confusion, 
it is necessary to make permanent mounts of interesting specimens. 
I have employed this method in teaching cHnical microscopy in 
the Medico- Chirurgical College, and beheve it to be ideal in its 
results. 

Washing Sediments. — Sediment collected at the bottom of 
the tubes by centrifugalization may be washed successfully after 
the following method : i . Pour off the clear supernatant urine, and 
to the sediment add sufficient water to fill the tube; then place 
the thumb over the mouth of the tube and invert it several times 
until the sediment is equally disseminated throughout the water. 
2. Place the tube (sediment and water) in the centrifuge and again 
sediment. 3. Decant clear supernatant fluid, continuing as above 
until the sediment has received three or more washings, when it 
will be cleansed and ready for mounting. 

Note. — Washing in no way alters sediments of dehcate struc- 
ture. 

If the sediment is to be preserved in crystalHne form, a drop of 
sediment is placed on the center of a slide and allowed to evaporate 
to dryness in the open air; a drop of Canada balsam or of the 
following mounting medium is placed on the center of the specimen 
by means of a glass rod, and a clean cover-glass allowed to fall 
gently on the medium, which is spread by its weight. Bubbles of 
air are in no way detrimental to the preservation of the specimen. 

Caution. — It requires a large drop of Canada balsam for 
mounting urinary sediment. 

Casts. — Renal casts are preserved by allowing the urine to 
evaporate nearly to dryness, a drop of the following medium 
being added to the center of the specimen: 

Liq. acidi arsenosi (U. S. P.) i jfl oz. 

Salicylic acid | gr. 

Glycerin 2 fl. dm. 

Warm slightly until solution is effected, when add acacia 
(whole tears), and again warm until solution is saturated; after 
subsidence decant clear supernatant Hquid. A drop of formaHn, 
40 per cent., may be added to this mixture. 

It will be noticed that the urine immediately surrounds the 
drop of medium, and in order to get the casts equally distributed 
throughout the slide it is necessary to carry a fine needle 
from the outer margin of the urine (wash- water and sediment) to the 
center of the medium until the two substances show no tendency 
to separate. A cover-glass is moistened by the breath and then 
allowed to fall gently upon the specimen. The slide is now put 



26o THE URINE. 

in a cool place for from twenty-four to forty-eight hours (see 
Casts, page 283), when it should be provided with a permanent 
ring of microscopic cement.* 

URINARY SEDIMENTS. 

It has been deemed advisable to divide all sediments of the 
urine, whether collected by allowing the urine to stand for several 
hours in a cool place or by the aid of the centrifuge, into two 
classes; viz., organic and inorganic sediments. 

The accompanying scheme will be found serviceable as a 
guide to the scientific research necessary for the determination of 
urinary sediments, and will refer the student to a more elaborate 
discourse upon the substance in question. 

INORGANIC SEDIMENTS. 

These may be either crystaUine or amorphous in character, 
and their physical properties will be governed largely by the 
chemic reaction of the urine in which they are found. The 
reaction — time since voided — and the naked-eye appearance of 
the sediment aid materially in making a positive determination, 
since one encounters crystals similar in microscopic appearance 
though widely different in composition. 

For convenience of study inorganic sediments are separated 
into two classes, viz., those found in acid and those occurring 
in alkahne urines. 

Acid urine, which on standing displays a heavy sediment of a 
reddish color, is suggestive of urates, and if entirely due to this 
substance, the turbidity disappears on heating (see Scheme, page 
261). When large crystals of uric acid are also present, we may 
observe fine, reddish-brown, sand-Hke particles at the bottom of 
the urine, and when the bottle is inchned so as to displace the 
urine, these sands may cling to its sides (see Uric Acid). A 
scarcely perceptible, flocculent precipitate seen near the bottom 
of the bottle suggests oxalates. Certain pigments from the blood 
and bile may at times discolor the urine and its sediments. 

Alkaline urine on standing is apt to display a more or less 
heavy sediment. When such sediment is easily broken by shaking, 
phosphates are probably present ; but when it is seen to be ropy 
and is not readily lifted into the pipet, pus and mucus may also 
be present. Heat increases the precipitate in either case, but 
turbidity due to phosphates disappears on the addition of acetic 
acid. Indican may be present in connection with a heavy sedi- 
ment and lend its color to the precipitate. 

* "N. Y. Med. Jour.," Nov. 4, 1899. 



URINARY SEDIMENTS. 



201 



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O 

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MD 



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(U ^ -t-> 






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oi u5 S 3^ ^ 

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< 5 Z D> 

z H <c/);> 



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^ •- oj .2 ^:2 S 

fT rj 'l- O O 3 i3 



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c3 



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m 



262 



THE URINE. 








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c 






T3 


a 


Cj 


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rt 


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S 










a 


-d 


r^ 






C flj r| w u U 

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a; ^ C 



o 'oj rj .2 



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Q Ph := g ^ ?- >^C^ 

^ Ci tl iri n-{ d >-* 






«^ _ o b 

-d u ^ 
15 



dj o J3 









^'of^ B 



-*=< ^ 

rt 

G a 



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0) 73 



cu;3-d "^ 23-^-2^ 



06 



^^ 



On 






,^ -::i ^ =3 
^H O -d -^ 



!U o 






g o a 

til 



S, o 

>. bo 



CJ 






3 o 



c -d 



w 



2 ^ 



o 

-d ^ 

=3 S 
o -^ 



^ a ^ 



^ £^g 



P > 



,i2 .ti qr; 



^3 



a Cfi id E W 
Ui W 0. H < 



t^ P fc S z 

5 b w p 

2: Z 7 o 

Z ^ *" h Qi J 

< >• U U J 

q; a; 05 Q Cu M 



°6 

'd 



^ u "L) 
t« :n D-'d 

u > a 5 

C "^—^ " 

rt ^ o -d 






c3 (^ 



^ 3Sfi ^ 



II 

o.t: 

I! 

. O 

o 



URINARY SEDIMENTS. 



26^ 






:2§2 

^ S y 



•G-= 2 36 



c3 w 



O 10 



*-. '^•^ O 



tT^ o 6 £i 






>.5 



en 



^•3 



lit 

- ^ y 
• rt j^ j^ 



S' 



c o 
b£) t« 13 



c o 






"e-J^ 















KM ^ c 5 






!? "^ (-( cj 4) ^-^ -^ 

u <s3 «3 +j t« ^-H u-)<i ro . 



'C ^ 



Gj u 






O O *- +J 

o oj bp fH 
"^-S-S bb 

t/3 -H rf O 



f-i ^, J-i 

O tj O 13 

V ^ ^ ^ 



.p4 






w ^ 



264 



THE URINE. 



Uric Acid. — Crystals of uric acid are originally colorless, but 
when present in urine they are colored yellow, brown, or red by 
urinary pigments, and specimens are seen extending through the 
successive variations of these shades. Rarely indeed are these 
crystals devoid of color in this situation. Crystals of uric acid may 
present many forms, and it is not uncommon to find two or more 
varieties represented in the same specimen, which necessitates that 
the student study many urines containing uric acid in order to be- 
come famihar with its many characteristic crystalHne forms. The 
accompanying plate (Plate 15) and illustration (Fig. 94) were 
sketched after a careful study of several slides — permanent mounts 




Fig. 94.— Uric acid. From selected slides (obj. Queen one-sixth). 



— collected from the author's clinical studies ; yet they fail to show 
many equally characteristic though not common crystalline forms. 
Crystals. — The size of these crystals varies greatly even in 
the same form. Among the commoner forms are : The irregular 
diamond shape (fiat-iron) crystal, which is often poor in coloring- 
matter and may present a central spot resembhng a nucleus or 
the outline of a smaller central diamond; rhombic plates with 
more or less rounded ends richer in color, thicker, more highly 
refractive, showing a distinct central spot and at times longitudinal 
striations (whetstone crystals) ; spheric or oval crystals from the 
surface of which project one or more spines; long forms presenting 
a rounded surface with a central diameter slightly greater than that 
of either extremity (cigar crystals); short, thick forms A\ith 



PLATE 15. 




Crystals of Uric Acid from Permanently Mounted Specimen Slides 
(obj. B. and L,. one-sixth; eye-piece 2). 



INORGANIC SEDIMENTS. 265 

abruptly broken ends and a central diameter far exceeding that 
of the extremities and at times displaying longitudinal and trans- 
verse lines (keg crystals); and rods of varying diameters clustered 
together, resembHng a bundle of arrows. Stellate and roset for- 
mations are common, and such crystals, when of large size, may 
give the appearance of the looping of a ribbon. Large and small 
amorphous masses characteristic only in color may constitute 
the only microscopic finding. 

Dilution and Recrystallization. — Crystals of uric acid are 
seen to dissolve, while under the microscope, if a drop of caustic 
potash be added to the slide, but are again crystallized as rhombic 
plates upon the addition of hydrochloric acid. 

Many crystals of uric acid may be found in urine which does 
not contain an excess of this substance, and one is not warranted 
in regarding the quantity of uric acid excreted abnormally high 
from microscopic study alone. 

Calcium Oxalate. — This substance when present in the urine 
may or may not be of pathologic origin; on the contrary, urine 
may contain an excess of unprecipitated oxalates which renders 
it necessary to estimate the oxaHc acid present in questionable 
specimens. Urine containing oxalates may be of nearly normal 
color, showing a finely flocculent sediment, situated a slight dis- 
tance above the bottom of the fluid and disappearing on the 
slightest agitation; but when present in connection with the prod- 
ucts of inflammation, the sediment is heavy. 

Solubility. — The crystals commonly observed are translu- 
cent envelops (Plate i6) which are seen to dissolve when 
treated with hydrochloric acid. Elliptic crystals of yellow tint, 
showing a central spot (nucleus) from which fine lines radiate, 
as well as large and small imperfect dumb-bells of a similar 
color, the isthmuses of which are surrounded by a faintly colored 
band (Fig. 95), are seen also. Less common are crystals not 
colored by the urinary pigment, but which appear as translucent 
bodies. Among this form are many biconcave discs, which when 
resting on their borders appear as minute dumb-bells, while their 
flat surfaces closely resemble red blood-corpuscles (Fig. 95). 
Larger crystals resembhng epithelial cells may accompany this va- 
riety. Colorless, diamond-shaped crystals with highly refracting 
centers may be found in connection with any of the above forms. 
Uric acid is common in urines containing oxalates. 

Clinical Significance. — It is difficult to interpret the true 
value of these crystals, as their presence is influenced largely by 
diet, exercise, and the general habits of the patient; and they occur 
in the urine of persons suffering from vesical calculus and pyeHtis. 



>66 



THE URINE. 



By some, oxaluria is regarded as a precursor of glucosuria. I 
have found these crystals common to the urine of persons over- 
fed and of sedentary habits, and where there is much mental strain. 




I^'g- 95- — Rare forms of calcium-oxalate crystals from case of plethora (obj. Queen one-sixth). 



Calcium Sulphate. — Crystals of this substance are among 
the rarer findings in urinary sediments. They occur as colorless 
needles and plates (Fig. 96), of variable thickness and length, with 

clearly defined borders and abruptly 
broken extremities. At times they 
unite to form bundles; and ill- 
defined dumb-bells are occasionally 
seen. 

Solubility. — Acids and ammonia 
cause no change in these crystals; 
they have been found in connection 
with triple phosphates and calcium 
carbonates (von Jaksch). They are 
of no known chnical importance. 

Calcium and Magnesitmi 
Soaps. — Crystalline soaps are 
formed probably from lime and 
magnesium salts of the higher fatty 
acids, and were first described by von Jaksch, who found them in 
the urine from a case of puerperal sepsis. I observed these sub- 
stances in the urine of three cases in the insane department of the 




Fig. 96.— Calcium-sulphate crystals from 
case of influenza. 



PLATE i6 




Dumb-bell Crystals of Calcium Oxalate with Uric-acid Crystals 
(Pennsylvania Hospital; courtesy of Dr. Cattell). 



INORGANIC SEDIMENTS. 267 

Philadelphia Hospital, with the following diagnosis : acute mania, 
hepatic abscess, and cocain poisoning. Dr. George Pfahler 
(through whose courtesy my studies were conducted) has made a 
detailed report of his findings in these cases.* 

Crystals. — These crystals appear in needle-like forms, and when 
studied singly under a moderately high-power objective (one- 
eighth) , are seen to taper decidedly at each extremity, while at the 
center two shght lateral depressions are observed (Fig. 97), which 
apparently favor their pecuHar arrangement. By careful focus 
and a feeble light the clusters (rosets) are found to be formed from a 
crossing of several of these needles, which focus at different levels 
so that when one layer is in focus the others appear indistinct 
and slightly shortened, giving somewhat the appearance of a 
chrysanthemum. Similar crys- _^— --,_, 

tals are found in feces. y^ "^ ^ 

These crystals do not re- / 

spond to the tests for tyrosin, 

and on careful study are seen : \ 

to differ widely from the crys- 
tals of that body, though im- 
perfectly formed sheaths are 
occasionally seen. 

Neutral Calcium Phos- 
phates. — This substance in 
the urine may appear as deli- 
cate, colorless prisms, and less 
commonly is it seen to take 
the form of fine needles, which 

may collect either in bundles magnesium. Shred of mucus in lower portion of 
/T->' r.\ • 1-1 field (from Pfahler 's case) (obj. B. and L. one- 

or rosets (Fig. 98), m which sixth). 

instance it resembles tyrosin. 

Such crystals occur in neutral or faintly acid urines, and are to be 

detected when such urines are changing from acid to alkaline. 

Solubility. — They are dissolved by acetic acid and by 
ammonia. 

Boric Acid. — After toxic doses of boric acid it may appear 
in the urine as an amorphous sediment. I am indebted to Dr. 
John A. McKenna for a specimen of such urine that was acid 
in reaction, cloudy, of high color, and showed a heavy sediment, 
which was composed for the most part of amorphous boric acid. 

Tyrosin and Leucin. — These substances when present in 
the urine in considerable amounts appear in the follov^ng crystal- 
line forms: 

*"Phila. Hosp. Rep.," 1900. 



X., 



Fig. 97. — Crystals of soaps of calcium and 



THE URINE. 



Tyrosin assumes the form of fine colorless needles of equal 
diameter throughout their length. They are commonly seen in 
bundles showing marked constriction at the center (sheaves)* 




Fig. 98. — Neutral calcium phosphate (obj. B. and L. one-sixth). 




Fig. 99.— Cn-stals of tyrosin from case of jaundice with enlargement of liver observed at 
Philadelphia Hospital (obj. B. and L. one-sixth). 



A sheaf may be broken at its center, and each half resemble an 
open fan (Fig. 99). These needles, when in alkaline medium^ 



INORGANIC SEDIMENTS. 



269 



occasionally unite to form rosets, resembling somewhat the 
soaps of calcium and magnesium, and of neutral calcium phos- 
phates, yet to the careful observer decided differences are ap- 
parent. 

Solubility. — By adding a drop of either an acid or an alkali 
to the slide, the crystals are seen to dissolve as they come in con- 
tact with these substances. Dissolution is also effected by heating 
the slide, when an odor of phenol is emitted. 

Clinical Significance. — Tyrosin being a product of the decom- 
position of proteids, appears in the urine in large amounts only 
when such changes are rapid, and is found in connection with 
leucin during the course of acute hepatic atrophy, acute phos- 




Fig. 100. — Leucin discs and tyrosin crystals (obj. Spencer one-sixth). 



phorus-poisoning, and rarely in sepsis, typhoid fever, leukocy- 
themia, small-pox, and other infectious maladies. 

Leucin. — Leucin is often found in the urine showing tyrosin, 
and is the result of similar retrograde metaboHc changes. Like 
tyrosin, but a small amount of this substance is crystallized to 
form a sediment, and it may be present in a comparatively large 
amount and yet give no microscopic evidence whatever. 

Leucin, when crystalline, occurs as small, highly refracting, 
yellowish spheres, slightly resembling oil-globules (see Figs. 100, 
loi ). Aggregations of these crystals in conjunction with amorphous 
material are common findings, and when pure, the crystals appear 



270 THE URINE. 

as extremely delicate plates; roset crystals are rarely seen in 
fresh urines, but standing encourages their development. 

Solubility. — Crystals of leucin are not changed by ether, which 
distinguishes them from the fat-globules. They are dissolved 
by caustic alkaHs. 

Bilirubin. — Urine containing large amounts of biHrubin may 
present this substance in crystalline form, which is seen either as 
rhombic plates or as fine needles and which may be distributed 
singly or in clusters varying in color from yellow to dark red. 
If a drop of nitric acid be added to the margin of the cover- 
glass and the specimen carefully watched while the acid enters 
beneath the glass and mingles through the urine, each crystal will 
appear to be surrounded by a greenish band. Crystals of bili- 
rubin are dissolved by caustic soda. 

Clinical Significance. — The urine from severe forms of jaun- 
dice may contain crystals of 
bilirubin which should always 
be distinguished from tyrosin — • 
a common finding in this situa- 
tion. 

Hematoidin. — UnHke biU- 
rubin, hematoidin assumes 
many crystalHne forms, rhombic 
or oblong plates, ill-formed 
^^ masses, small discs from which 
@ fine needles are seen to radiate, 

Fig. loi.-Leucin crystals (Ogden). and occasionally a crystal re- 

sembHng the hmb of a tree, 
displaying fine branches on one or both sides (Plate 17). Their 
color is red and varies according to the shade of the urine in 
which they are suspended. 

Distinction. — When treated with impure nitric acid, a play of 
colors is observed changing to a transitory blue. Bilirubin 
when thus treated changes to green. Bile-pigments, too, rarely 
display a blue color, which therefore renders the nitric-acid test 
of httle use with biliary urines. 

Solubility. — Crystals of hematoidin are insoluble in acetic 
acid and partially soluble in ether. 

Clinical Significance. — Hematoidin may be found in the 
urine during the course of acute infectious fevers, acute yellow 
atrophy (hepatic), phosphorus-poisoning, jaundice, hepatic cirr- 
hosis, or carcinoma, and following the rupture of vessels or 
abscesses into the urinary tract; and after renal trauma.* 

* Yarrow, "N. Y. Med. Jour.," Jan. 6, 1900 





PLATE 17. 




Hematoidin Crystals and Filaria Sanguinis Hominis from the Urine. 



INORGANIC SEDIMENTS. 



271 



Through the courtesy of Dr. John A. McKenna I was provided 
with a number of specimens of urine from a patient from whom 
one kidney had been removed and which was found by the surgeon 
to consist, for the most part, of a cyst or of an abscess ( ?) contain- 
ing milky fluid. The urine in addition to showing many crystals of 
hematoidin also contained a few small parasites (not determined) 
(Plate 17) which were lifeless. 

Triple Phosphates. — Crystalline ammoniomagnesium phos- 
phates are to be found in feebly acid specimens (see Alkaline 
Sediments, page 275). 

Solubility. — Crystals of phosphates are readily soluble in acids. 

Basic Phosphates of Magnesium. — Urines found to be 
faintly acid, alkahne, or neutral in reaction at times contain this 
substance in crystalline form, 
when it appears as highly 
refracting, elongated rhombic 
plates resembling somewhat 
the envelops of calcium oxalate, 
but they are more massive 
and less perfect. Again they 
are seen to resemble a clover- 
leaf in form. 

Solubility. — They are dis- 
solved by acetic acid and may 
be reprecipitated on the addi- 
tion of sodium carbonate. No 
special clinical value is at- 
tached to their presence. 

Hippuric Acid. — This sub- 
stance is rarely present in 

human urine, and is said to follow the ingestion of cranberries 
or the administration of benzoic acid. Its crystals are colorless, 
four-sided prisms, soluble in both hydrochloric acid and ammonia. 

Cystin. — Urine containing cystin is not apt to be decided in 
reaction, and if a considerable amount be present, it is Hkely, 
on standing, to emit an odor of sulphureted hydrogen. It does 
nor follow, however, that such urine will always give microscopic 
evidence of this substance in its precipitate. The addition of 
acetic acid causes cystin to be thrown out of solution, and appear 
in the form of colorless, hexagonal plates with clearly defined 
margins (Fig. 102). 

Solubility. — They are soluble in ammonia and hydrochloric 
acid, but unaffected by alcohol, ether, acetic acid, and water. 

Clinical Significance. — The urine contains cystin in the 




Fig. 102.— Crystals of cystin. Study through 



the courtesy of Dr. J. M. 
L. one-sixth). 



Anders (obj. B. and 



272 THE URINE. 

presence of vesical calculi formed from this substance, and cystin- 
uria may persist after the removal of such calculus. 

Xanthin. — This substance must indeed be rare, Purdy 
estimating the total number of cases reported at less than one 
dozen. Morphologically, crystals of xanthin resemble those of 
uric acid, but are colorless. A noteworthy fact, however, is that 
colorless crystals of uric acid may be seen. Chemic analysis 
is therefore necessary to decide between these two substances. 

Cholesterin. — Urine containing this substance is feebly acid, 
as a rule, and of normal color or slightly turbid. On standing, 
the precipitate contains the characteristic crystals (Fig. 92), and 
when it is disturbed by shaking, fine, scale- like flakes are seen to 
float in the Hquid. Under the microscope these crystals appear 
as thin, translucent, glassy plates, often overlapping one another. 
Clinical Significance. — Urine containing chyle, and where 

certain cysts — hydatid or others — 
have communicated with the genito- 
urinary tract, may show cholesterin. 
Acid Ammonium Urates. — 
Occasionally we find crystals of 
ammonium urates in acid urine, 
but in such instances the urine 
contains an unusually large amount 
of amorphous urates or other sedi- 
ments common to acid urine, as 
oxalates. When urine is but feebly 
acid, and during the change from 
Fig. io3.-Acid ammonium urates from acid to alkali, — the result of stand- 

case^of rheumatism (obj. Queen one- i^g,— typical SphcrCS and chcstnut- 

burr (thorn-apple) crystals may be 
seen. In fresh acid urine, urate of ammonia appears in the form 
of spheres from which project one or more spines, often parallel 
to one another, with sharp or blunt points, and appear to 
be formed from a coarsely granular substance (Fig. 103 and 
Plate 18). Many of these crystals unite to form huge, dark- 
brown or yellowish masses, showing blunt, spine-like projections 
which are seen at different points of focus. Chains formed 
of from three to five perfect spheres, ha\dng the appearance of a 
segmented block v^th rounded ends, — by far the most common 
forms of crystals of acid urates, — are often present without the 
above forms. Again, there are bottle-shaped crystals which 
may be clustered (Plate 18), and less often rosets composed of 
four or more spheres are seen ; but true dumb-bells are rare. All 
the above forms are more or less deeply colored, varying from a 




PLATE 




Acid Ammonium Urate (from a case of chronic rheumatism studied in 
the Pennsylvania Hospital). 



INORGANIC SEDIMENTS. 



273 



light yellow, in the smaller varieties, to yellowish brown in the 
larger forms. 

Clinical Significance. — Rieder reports having studied these 
crystals from a single case. I have observed them in fresh 
acid urines on four occasions: One being found in a case of 
rheumatism treated at the Pennsylvania Hospital; another, with 
a diagnosis of gout, was studied through the courtesy of Dr. 
Henry Cattell; and the remaining cases gave histories of rheu- 
matism and were observed at the Philadelphia Hospital, one suf- 
fering from acute alcoholic delirium, the other from acute mania. 
The segmented block and the bottle-crystals I have seen in 
the urine of tonsillitis and of acute articular rheumatism. 




Fig. 104.— Sodium-urate crystals from urine of a gouty patient observed at Pennsyl- 
vania Hospital (obj. Spencer one-sixth). 



Acid Urate of Sodium. — The greater portion of this substance 
appears in the urine as granular debris, but crystals may also be 
seen (Fig. 104) in the form of fine needles (Fig. 105). These 
needles may unite to form imperfect sheaves, which, when broken 
into halves, have the appearance of an opened fan. They are 
originally colorless, but may be colored by the urinary pigments, 
and are therefore the same shade as the urine from which they 
are precipitated. Acid urate of sodium enters into the formation 
of sediments containing uric acid. 

Solubility. — It is soluble in 124 parts of boiling water and 
II 50 parts of cold water (Purdy). 
18 



274 



THE URINE. 



Amorphous Deposits.— Urates.— This variety of urates is 
a common cause of the highly colored turbidity of urine from 
plethoric and febrile conditions (tonsillitis) ; but when gentle heat 
is applied such turbidity disappears. Microscopically, this sub- 
stance appears as small granules arranged in masses, which 
under a one-sixth objective present a slight yellowish tinge. 
Such sediment when treated with acid may precipitate rhombic 
plates of uric acid. 

Calcium Sulphate and Oxalate. — Both of these substances 
may appear as irregular dumb-bells accompanied by a variable 
amount of amorphous material. Sulphates are insoluble in 




Fig. 105. — Crystals of a complex urate (?) which crystallized on cut surface of a gouty 
node that had been removed from a toe ; observed at Pennsylvania Hospital (obj. Queen 
one-sixth). 



concentrated hydrochloric acid, which dissolves the oxalates. 
Oxalates are insoluble in acetic acid. 

Fat. — Highly refractile bodies of varying size are always 
suggestive of oil-globules. They are soluble in ether, and stain 
pink or red when treated with Sudan III, or black with osmic acid. 

Clinical Significance. — Fat may appear in the urines of para- 
sitic chyluria, phosphorus-poisoning, and chronic Bright's disease 
with fatty degeneration of the heart. 

Dark Bodies. — Many dark amorphous bodies are seen in 
the urines of jaundice, hematuria, and fevers. Such findings 
have been described under their respective headings, and one 
must rely on chemistry to determine their true composition. 



INORGANIC SEDIMENTS. 



275 




Fig. 106.— Crystals of phosphates (obj. B. and L. one- 
sixth). 



Acid Calcium Urate. — This is a rare urinary deposit and 
appears as a whitish or grayish powder, which is dissolved with 
difficulty; and from 
which, when fused, a 
white residue of calcium 
carbonate remains. 

Acid Potassium 
Urate. — This substance 
forms part of the amor- 
phous deposit seen in 
acid urine. It is more 
soluble than is acid cal- 
cium urate. 

Crystalline Sedi- 
ments from Alkaline 
Urine . — Triple Phos- 
phates. — This sub- 
stance (crystalline am- 
moniomagnesium and 
calcium) when crystal- 
lized from urine may 
assume many forms, which vary with the degree of alkalinity and 
whether or not such alkahnity is the result of ammoniacal fermen- 
tation. Most constant 
are the cofhn-Hd and 
building-stone crystals 
(Fig. 106); yet many 
other forms are seen, 
among them being 
the clothes-pin crystal 
(Fig. 106) and the 
feather crystal (Fig. 
106), which at times 
resembles the fin of a 
fish, and which, when 
so broken as to permit 
a view of the ends 
of the fin's ribs, re- 
sembles a number 
of rounded timbers 
standing on their ends, 
for w^hich reason I 




Fig. 107.— Crystals of phosphates from a case of phos- 
phaturia (obj. Queen one-sixth). 



have presented it to 
my students as the "pile crystal"— resembling the group of piles 



276 



THE URINE. 



which project from the end of a wharf. A crystal bearing like- 
ness to the reel used by fishermen is occasionally seen ; as are also 
heavy, step-like blocks of varying sizes (Fig. 106). Square, oblong, 
irregularly jagged, snow-flake, and leaf-like forms are also among 
the findings. 

Solubility. — Acids are usually destructive to triple phosphate 
crystals from alkahne urines. 

Clinical Significance. — Flatulent dyspepsia may cause a deposit 
of calcium phosphate from mixed alkaH. Constipation and 
certain nervous affections, phosphatic vesical calcuH, and cystitis 
contribute toward phosphaturia. It is not possible to estimate the 
amount of phosphates from microscopic study alone (see page 181). 

Urate of Ammonium. — This substance is commonly crystal- 
Hzed from urines of high specific gravity, displaying a sediment 




Fig. 108.— Ammonium urates, showing segmented bottle-crystals and thorn-apple formation. 



containing calcium phosphate and triple phosphates in addition; 
while urines of lower density are apt to precipitate their urates in 
the form of uric acid; however, ammonium- urate crystals may 
be present in urine of low specific gravity. 

The most constant crystal of this substance is a small, yellowish 
brown sphere. These spheres are seen singly or in groups of four 
to six, when they form a crude roset. Smaller spheres occur 
in pairs connected by an isthmus (dumb-bell); large spheres 
showing one or more small spines projecting from their surfaces 
(chestnut-burr or thorn-apple) are also seen. These spicules 



INORGANIC SEDIMENTS. 277 

may be straight or slightly curved (Fig. io8), and rarely are they 
seen apart from spheres. Crystals of ammonium urate are dis- 
tinguishable from those of uric acid, acid urate of ammonium, 
and sodium urate by the fact that they are the only urate crystals 
found in alkahne urine. 

Solubility. — They are dissolved by phosphoric and acetic acids, 
after which they may precipitate as rhombic plates of uric acid. 

Indigo. — It is common for indigo to appear in the urine 
as amorphous debris, and needle-Kke crystals showing a bluish 
tint are occasionally seen. They are formed probably from 
indoxyl sulphate during the process of decomposition. Crystals 
of indigo may be found in either acid or alkaline urines, and in 




Fig. 109.— Crystals of calcium carbonate (obj. Spencer one-sixth). 

form varying from that of needles to oblongs and squares; their 
shape being modified by the crystals or debris upon which they 
are collected. 

Clinical Significance. — Indigo when found in the urine is a 
symptom of cholera, empyema, neoplasm, conditions favoring 
intestinal putrefaction, constipation, peritonitis, tabes dorsaHs, 
jaundice, and general cachexia. 

Amorphous Alkaline Deposits.— Carbonate of lime occurs 
in the urine in coarse granules and as colorless dumb-bells (Fig. 
109) and evolves gas when dissolved in acetic acid. Carbonates of 
alkaline earths are dissolved without the evolution of gas. 

Basic phosphatic earths occur as large and small granular 



278 THE URINE. 

bodies, which, when treated with acetic acid, generate gas during 
their dissolution. 

Urinary concretions are often apparent to the naked eye, 
and may consist of uric acid, phosphates, cystin, oxalates, xanthin, 
carbonates, and cholesterin. These will be discussed under their 
respective heads. 

ORGANIC SEDIMENTS. 

Leukocytes. — A few isolated leukocytes are present in normal 
urine, but when present in large numbers they are of pathologic 
origin. They are often increased after the worship of Venus and 
Bacchus, though in such urines they are well preserved and pre- 
sent clear nuclei and their usual smooth and glossy appearance. 
Leukocytes when present in alkaline urine soon become 
lusterless, swollen, and their nuclei become indistinct. By 
placing a drop of acetic acid at the margin of the cover-glass and 
watching the specimen closely through the microscope, it will be 
seen that all cells coming in contact with the acid at once display 
more clearly their nuclei. Add a drop of iodopotassic-iodid 
solution in place of the acid, and the leukocytes stain a faint 
mahogany shade which serves to distinguish them from epithelia, 
which stain yellow. Pus-cells, when treated with Hquor potassa, 
show a tendency to swell and coalesce, their nuclei being seen with 
difficulty. 

Clinical Significance. — The leukocytes of the urine may be 
derived from any portion of the urinary tract through conges- 
tion, or from abscesses of adjacent structures rupturing into the 
urinary channel. It is the rule that when a Hmited number of 
pus-cells are found equally distributed through the urine, they 
are of renal origin (pelvic) ; while a large or small amount of pus, 
not thus disseminated throughout the urine and found in con- 
nection with large epithehal cells, may be regarded as being of 
cystic origin. 

Pus. — The pus of purulent catarrh of the bladder and of acute 
urethritis (gonorrhea) forms a heavy \iscid sediment, and the cellu- 
lar elements are commonly much distorted. 

Pus-cells occur in the urine in case of inflammation of the 
ureters and in pyelitis, but here the sediment is less marked (Fig. 
no) and often has a light, flocculent appearance, while that from the 
bladder is ropy and not readily broken into floccuh by shaking. Pus 
from abscesses may resemble that of cystitis except for the par- 
ticles of fatty matter seen in occasional cells. It is to be remem- 
bered that in renal disease often but few leukocytes are to be ob- 
served, and that in women they may be of vaginal origin. To 
determine the source of the pus in the urine is of the greatest 



ORGANIC SEDIMENTS. 



279 



clinical value, and may at times be done with a certain degree of 
accuracy, the exceptions being no less numerous than the rule. 
Catheterization of the ureters has been proved of service in my 
experience. 

Epithelia. — The deposit which forms in normal urine contains 
a few epithehal cells, most of which are of the squamous variety, 
yet smaller forms may be present, since desquamated epithehum 
is a product of all mucous surfaces. 

Clinical Significance. — Both polygonal and round uninuclear 
cells are derived from the prepuce, meatus, and vagina; while 




Fig. no.— Urinary sediment from case of pyelitis : i, Epithelial cells, probably from pelvis of 
kidney; 2, large pus-cells ; 3, small pus-cells (obj. Spencer one-sixth). 



epithelial cells from the bladder are usually flat, irregularly round 
or angular, the nucleus located nearly central, and is seen without 
staining (Fig. in). The epithehal cells from the ureters and 
renal pelvis are, as a rule, of medium size and often display a 
caudal projection (Fig. in, 2). Marked difference is observed be- 
tween epithehal cells from the superficial and deeper layers covering 
any mucous surfaces. Small cells, and also those showing tail-hke 
projections, were formerly regarded as coming from the kidneys 
or renal pelvis, but careful study has shown that cells identical 
in every respect may originate from the deeper layers covering 
the vesical mucosa. 

When urinary sediment contains a large number of epithehal 
cells characteristic of any portion of the urinary tract, it may be 



28o THE URINE. 

inferred that there is an inflammatory process affecting such 
sections. Where cancer affects these parts, clusters and nests of 
epithelial cells appear in the urine. Many caudate cells are 
significant of pyelitis, although such cells may be the product of 
cystitis. In a sediment containing many small epithelial cells 
resembling pus-cells (see Pus^ page 278), where the urine contains 
albumin, or following infectious fevers (scarlatina), one may 
safely regard such cells as of renal origin. Casts often contain, 
and may often be found largely composed of, these cells (see 
Epithelial Casts, page 288). 

Disease may alter the general feature of the epithelium, and 
while epithelium from the kidney is fairly common, the presence 
of such cells in the urine may not bear a direct relation to the 





* 










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/ 




r" 


^i ^-:. ^- 


'(■.' 


v^-^ 


,/ 


^m ■' , 


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Fig. III. — I, Epithelial cells from the bladder; 2, from kidney, pelvis of kidney, and fron> 
ureter; 3, cells from meatus of male urethra (obj. B. and L. one-sixth). 

degree of pathologic condition present. I have been privileged 
to follow to autopsy many cases of nephritis, and of amyloid 
kidney, and have found that the number and character of the 
epithelial cells present in the urine did not bear a direct relation 
to the lesion present, and at times their number may bear in- 
verse proportion to the apparent damage of the kidney's 
structure. They were commonly present singly and in clusters 
(three to six cells each) in cases of toxic nephritis (acute yellow 
atrophy). Cells showing fatty and amyloid change point with a 
variable degree of certainty to similar changes in the kidney's 
structure, yet by no means is this finding constant or even common 
at postmortem. 

Our present knowledge in no way warrants the determination 
of the origin of any given epithelial cell present in the urine; 
but in connection with the clinical features of a given case such 



ORGANIC SEDIMENTS. 28 1 

deductions may be drawn with safety (see Epithelial Casts, page 
288). 

Blood (Hematuria).— Red blood-cells appear in the urine as a 
result of pathologic changes, either in a portion of the urinary tract 
or in the blood itself (see Malaria, Filaria Sanguinis Hominis, and 
Distoma, pages 153, 147, 147). Blood-corpuscles vary in their 
general characteristics (see Erythrocytes, page 81), depending on 
the portion of the urinary tract from which they are derived, and 
the reaction and consistence of the urine in which they are found 
(see Osmotic Tension, page 73). Blood- corpuscles derived from 
the kidneys rarely increase the specific gravity, are equally distri- 
buted throughout the urine, never form rouleaux, and retain their 
form well if the urine be acid ; but in alkahne urine they become 
swollen, showing slight color, and, should the urine be diluted, ap- 
pear as mere rings. They present deep color and thickening 
where the urine is concentrated. Corpuscles derived from the 
renal pelvis display these peculiarities to a lesser degree. 

Clinical Significance. — Blood from any portion of the uri- 
nary tract causes a change in both the color and sediment of 
the urine, bearing a direct ratio to the quantity of this tissue 
present. It causes a dark-red color in acid urine and a bright- 
red hue where the urine is alkaline. Blood derived from the 
renal substance and pelvis lends to the urine a general cloud or 
tint, while that from the urethra, bladder, and other portions of 
the urinary tract is not found to be equally diffused throughout the 
urine, and it forms a heavy sediment, clots readily, or may even be 
voided in clots. 

Hematuria may result in the course of severe anemia (leukemia) 
or of certain infectious fevers, either as the result of renal congestion 
or of an altered condition of the blood itself (malarial hematuria). 
It may develop as the result of acute nephritis, renal abscess, 
tuberculosis, calculi, pyeHtis, cystitis, urethritis, trauma, and a 
complication in cardiac and hepatic conditions. Tropic hema- 
turia may be produced either by the distoma (page 147) or by the 
filaria (page 147). 

Other animal parasites capable of causing bloody urine are : T. echinococcus, 
Oxyuris vermicularis, ascarides, Rhabditis genitalis, Trichocephalus, Anguillula 
aceti, and the ameba (pages 292-300). Infection of the genito-urinary tract by 
the various vegetable parasites (fungi and bacteria) may often induce hematuria 
(pages 300-307). 

Sloughing mucous surfaces located along the urinary tract, urethral stricture 
and inflammation are among the rarer causes. 

When taken into the system, drugs may induce hematuria. 
The urine may display peculiarities, such as odor, color, or chemic 
changes, all of which are equally suggesdve of the cause. 



262 



THE URINE. 






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CASTS (tube-casts; renal casts). 283 

CASTS (TUBE-CASTS; RENAL CASTS). 

History Note. — The presence of renal casts in the urine was 
first described by Vigla*; and Henlef called attention to their 
presence in the urine of persons suffering from dropsy. 

Formation. — Different theories have been offered as to the 
method of their production; but the one generally accepted is that 
coagulable elements of the blood enter the urinary tubules as a 
result of pathologic changes (irritation), and there serve as a base- 
ment lining of the tubule, forming a favorable lodging-place for 
all granular material that may enter the tubule either at its union 
with the Malpighian body or that may exude from the tubule's 
wall, or from the structural hning of the tubule itself. Thus a 
cast may displace different cellular elements, suggestive of the 
changes taking place in the tubule of which it is a mold. 

Composition. — The substance forming the basement or 
primary mold of casts is closely allied to proteids, but its true 
nature is not known. Knoll, after careful study of the chemistry 
of casts, concludes that their composition is not identical with 
any known proteid, though waxy casts at times give reactions 
known to albuminates. In hyaHne casts this substance is freely 
soluble in dilute mineral acids. 

Clinical Significance. — Our present knowledge regarding 
the clinical significance of urinary casts is such as to render this 
subject one of great interest. Casts are commonly found in 
urines that appear normal in other respects and when albumin 
is not present; but such urines are usually voided after rest 
or sleep. A specimen collected after exercise, or two hours 
after a full meal, etc., will, as a rule, show albumin in ad- 
dition. In all such cases under personal observation, in which 
a more careful investigation was conducted and specimens col- 
lected at different hours of the day, albumin was always detected, 
though often in small amounts. The more closely we study this 
class of cases, the more we are inchned to regard them as related, 
at least, to true nephritis, which, if not present, will develop later. 
The finding of casts in the urine may be regarded as pathologic and 
significant of nephritis when the slightest trace of albumin is 
detected two hours after an evening meal, the day having been 
spent in taking a reasonable amount of exercise. 

Classification. — For clinical study renal casts may be classi- 
fied as follows: unorganized and organized. 

Unorganized casts are formed of crystalHne or amorphous 

* " L'Esperience," 1837, No. 12. 

t " Zeitschr. f. rationelle Med.," 1844, vol. i, pp. 61-68. 



284 THE URINE. 

substances; and are composed of urates in gouty individuals and 
in case of renal congestion. Casts of hematoidin crystals have 
been seen. 

Organized casts are composed largely of cellular elements or 
their products, and may be classified according to their composi- 
tion, frequency of occurrence, and method of production : 

1. HyaHne casts, which appear as thin, pale molds of the renal 
tubules. 

2. Granular casts, by far the most common, are composed 
largely of degenerated cellular elements and granular debris. Amy- 
loid, fatty, pus, and blood-casts are subdivisions of this variety. 

3. Casts consisting largely of red blood-cells, epithehal cells, 
leukocytes, or bacteria. 

4. Composite casts, where the larger portion is hyahne, but 
shows at certain sections granulations due either to cellular ele- 
ments or to crystals. 

5. False casts (cylindroids), which resemble in certain respects 
hyahne casts but display distinctive features not knowm to casts. 

The size and form of casts are best shown by the accompany- 
ing figures and plate (Figs. 11 2-1 20 and Plate 19), which demon- 
strate their marked variations and general characteristics. This 
variation is at times so marked as to cause those most skilled in 
their recognition to question the true nature of many bodies 
found in urinary sediment. Abnormally large casts often take 
the form of the tortuous tubules, while on the other hand narrow 
casts may be perfectly straight and of moderate length. Age has 
no influence upon the size of casts, as show^n by Fig. 115, from 
the urine of a child (girl) four years old, under the care of Dr. J. 
Allison Scott, and observed during my service at the Pennsylvania 
Hospital. 

Staining of Casts. — Casts are stained by bile when present in 
biliary urine. lodin added to the urine stains the casts feebly 
but stains the other elements more markedly and thus renders 
them (casts) conspicuous; and a similar effect results from anihn 
dyes. 

Urate Casts. — This variety of casts (Fig. 112) is commonly 
met with in general uranalysis. They appear to be composed of 
amorphous urates. At times they closely resemble organic granu- 
lar casts, in which case an absence of urates suffices for differenti- 
ation. Rarely are organic casts seen in the same urine with weak 
casts. When urate casts meet they show a tendency to coalesce, 
forming an unorganized mass — a condition not observed if the 
casts be composed of organic substances. 

Their presence in the urine is probably suggestive of renal con- 



CASTS (tube-casts; renal casts). 



285 



gestion. The author has found them common in cases of ple- 
thora, rheumatism, and tonsiUitis. Two women of middle life, 
now under observation, develop periodic attacks of tonsiUitis, at 
w^hich time their urines contain many such casts. Between these 
attacks the urine is normal. Urine containing such casts develops 
a heavy sediment on standing and may present a cloud even when 
voided (see Transparency, page 171). 

Casts composed largely of hematoidin crystals have been ob- 
served by various writers. 

Hyaline Casts. — There is a diversity of opinion as to the 
method whereby this primary variety of casts is produced, some 
regarding their formation as due to a special product secreted by 
the renal epithehum, while others contend that they are formed 





Fig. 112.— Urate casts (pseudo-casts) 
from case of tonsillitis. Renal epithelia 
and leukocytes (obj. B. and L. one-sixth). 



Fig. 113. — Hyaline casts showing fat-droplets 
and leukocytes (obj. B. and L. one-sixth). 



from albumin or its derivatives, which escapes into the renal 
tubules. 

Hyaline casts appear in the urine in variable numbers and are 
of indefinite proportions. Wide variations exist as regards the 
diameter of these bodies, and they may vary in length from one- 
fourth to several times the diameter of a microscopic field; their 
outline is faint and seen with difiliculty, and one extremity occa- 
sionally presents a twisted appearance or shows slight tapering. 
The surface is finely granular and displays not infrequently epi- 
thelial cells, leukocytes, or crystals (Fig. 113). Casts of similar 
composition, but larger, are observed in puerperal eclampsia 
(Plate 19). 

Detection. — Hyaline casts are most difficult of detection and 
are seen only when the most skilled tcchnic is employed in adjust- 



286 THE URINE. 

ing the mirror and diaphragm. The interposing of a colored glass 
between the mirror and the condenser of the microscope is of ser- 
vice. They may appear quite distinct under a low-power objective 
(two-thirds), but at the same time it is difficult to see them when 
highly magnitied. Staining is often recommended, but in my 
experience this method of study has proved valueless. 

Clinical Significance. — Various writers claim to have found 
hyaline casts in the urine from perfectly healthy persons, and 
in cases where postmortem disclosed a healthy condition of the 
kidneys. I wish to add my experience to that of Leube and Purdy * 
in that urine containing hyaline casts contains albumin or has re- 
cently contained this body, even though in small amounts. Study 
of a series of similar cases at the Howard and Philadelphia Hospi- 
tals resulted in the detection of albumin, at some period, when it 
was possible to follow the cases and make examinations at inter- 
vals of days or even weeks, and of 
urines collected at different hours of 
the day, after exercise, a full meal, 
etc. This variety of cast is most 
commonly found in chronic neph- 
ritis of the interstitial type ; it occurs 
also in other forms of chronic and 
less often in acute nephritis, catar- 
rhal jaundice, cancer of the liver, 
stomach, or intestine, and in condi- 
tions coupled with anemia. At times 
casts are stained, due to the presence 
from^ase"l7o?t^lc"edSni"^^p°oS of bilc-pigmcnts in the urinc (Plate 
mortem observed at Philadelphia H OS- ig). Hyaline casts are not uncom- 

pital (obj. B. and L. one-sixth). ^^ J 

mon during the latter months of 
gestation and in puerperal eclampsia (Plate 19). The urine 
may contain hyahne casts for many years (Fig. 114) (ten to thirty) 
without pronounced albuminuria or appreciable discomfort to the 
patient. 

Granular Casts. — This variety comprises by far the greater 
portion of all renal casts, since epithelia, pus, leukocytes, and blood- 
casts are subdivisions of this class. Granular casts are largely 
composed of the products of pathologic changes which have be- 
come disorganized while in the uriniferous tubules. They are 
seen to vary greatly in size and general characteristics, depending 
upon the nature of the existing renal lesion, the time they have 
remained in the renal tubules, and the degree of acidity of the urine- 
in which they are found, alkaline urine causing them to disinte- 
grate. 

* "Zeit. f. klin. Med.," 1887, vol. xiii, p. 7. 




PLATE 19. 



Various Forms of Urinary Casts. 

1. Hyaline casts from case of puerperal eclampsia (original) (obj. B. and L. one- 
sixth). 

2. B. J., age twenty-two, female, suffering from puerperal eclampsia. Urine 
showing large, finely granular casts (original) (obj. Queen one-sixth; eye-piece 2). 

3. S. A., age fifty-eight, male. Urine showing granular and fatty casts; post- 
mortem showed chronic parenchymatous nephritis (original) (obj. Queen one- 
sixth; eye-piece 4.) 

4. J. D., age fifty-four, male, suffering from cancer of the common duct and 
head of the pancreas. Urine showed bile-stained casts (original) (obj. Queen 
one-sixth; eye-piece 4). 

5. A. G., age fifteen, male, suffering from acute nephritis. Urine showed 
granular casts (original) (obj. Queen one-sixth; eye-piece 2). 

6. C. A., age nine, male. Scarlatinal nephritis, third week of convalescence. 
Urine showed granular casts (original) (obj. Queen one-sixth; eye-piece 2). 



CASTS (tube-casts; renal casts). 



287 



Granular casts present in common certain features (Plate 19) : 
Either one or both extremities is seen to have been broken abruptly 
or obliquely, often causing a concave or zigzag fracture; or one 
extremity may taper slightly. Their lateral boundaries appear 
as slightly irregular, elevated borders which vary according 
to the variety of granulation presented by each cast. Such casts 
differ in their constitution: at times their granules are coarse and 
dark, and again so fine and pale as to be seen only through a 
one-sixth objective. The latter may show fine crystals, epithelial 
cells, leukocytes, fat-globules, or crystals of fatty acids on their 
surfaces (Plate 19). In color, granular casts extend through 
the successive shades varying from a faint yellow to a reddish 
brown or a bluish yellow. 

Clinical Significance. — It is 
the rule that highly granular 
casts are short, thick, and com- 
monly found in connection with 
acute renal inflammation; yet 
the exceptions are many. 
Large finely granular casts are 
observed in puerperal eclamp- 
sia and chronic parenchymat- 
ous nephritis ; while the narrow 
variety is suggestive of chronic 
interstitial disease. The variety 
of granular casts present in the 
urine offers valuable aid in de- 
termining the exact nature of 
the renal condition present, 
except where the patient be 

suffering from an acute exacerbation, relative to some form of 
chronic nephritis, in which case the casts signify acute nephritis. 

Blood-casts. — Generally speaking, blood-casts are short, of 
uniform diameter, and their margins distinct. When formed of 
a small quantity of blood-cells, they are light in color and 
each corpuscle may be outlined by careful focus, but where 
the renal hemorrhage has been sufficient completely to fill the 
tubule and to form a mold purely of compressed red cells, they 
are dark in color and of varying sizes (Fig. 115). Blood-casts are 
not destroyed in evaporating the sediment of the urine to dryness, 
and can, therefore, be mounted in Canada balsam. 

Caution. — In urine containing a large amount of blood the 
thickest of its sediment should not be taken for microscopic study, 
as blood-casts are more easily found in the sediment obtained 




Fig. 115. — Blood-casts and crystals from 
urine of a child at Pennsylvania Hospital 
(courtesy of Dr. A. Scott) (obj. Spencer one- 
sixth). 



288 



THE URINE. 



from the supernatant portion of the fresh urine which renders 
centrifugation of such urines necessary. 

Clinical Significance. — Blood- casts are indicative of renal 
hemorrhage, but do not imply that permanent structural change 
has taken place in these organs. They are a rather common 
feature of the urine of acute traumatic and of toxic nephritis. 
Figure 125 illustrates blood- casts from a case of hydatid of the 
kidney studied at the Philadelphia Hospital.* 

Epithelial Casts. — The characteristic feature of this variety 
of casts is that they are formed entirely, or in part, of epithelial 
cells from the lining surfaces of the renal tubules. They are of 
moderate size, highly refractive, and often so broken as to allow 
a portion of an epithehal cell to extend beyond the extremity (Fig. 
116); the margins are irregular, and their surface may present 

a few epithehal cells scattered 
throughout, or an aggregation of 
such cells at any point, while the 
remaining surface appears finely 
granular or rarely hyahne. Casts 
may be seen when a row of epithe- 
lial cells surrounds them in a spiral- 
like manner, giving the appearance 
of the thread of a bolt (Fig. 116); 
again, the free surface may be en- 
tirely covered with epithelial cells, 
which may be granular, swollen, and 
indistinct, presenting rather poorly 
defined margins (Figs. 118, 119). 
Clinical Significance. — Epithe- 
lial cells containing fat-droplets, and showing marked e\ddence 
of degeneration, are to be seen and are fairly suggestive of the 
presence of a similar condition in the kidney structure. 

The finding of epithehal casts in the urine furnishes conclusive 
evidence of an inflammatory process in the kidneys which is of 
sufficient severity to destroy the epithehal Hning of the urinary 
tubules. It is a common feature of the exanthemata (scarlet 
fever), but does not of necessity imply that the kidneys are per- 
manently damaged. 

Pus-cells. — It is common to see granular, amyloid, and hyaline 
casts upon the surface of which a few leukocytes are chnging; 
and casts composed of pus-corpuscles have been described 
by Johnson, and observed by the author in a single instance — a 
case studied through the courtesy of the late Dr. H. E. Gruel 

* "Amer. Med.," Jan. 3, 1903. 




Fig. 116. — Epithelial casts from a 
case of acute scarlatinal nephritis. Pri- 
vate patient (obj. B. and L. one-sixth;. 



CASTS (tube-casts; renal casts). 



(Fig. 117), where the sediment was more fiocculent and lighter in 
color than is that resulting from pus of vesical origin. 

Clinical Significance. — Dr. Gruel's patient died of uremia 
within a few hours after the specimen was collected, and no 
autopsy was permitted. 

Fatty Acids. — Casts showing scattered globules of fat on their 
surfaces are rather frequent findings, and occur in connection wdth 
the amyloid and hyaline varieties found in subacute and chronic 
nephritis. Aggregations of fatty matter may present needle-like 
crystals (Plate 19) which doubtless have their origin in the degen- 
erated renal epithelia. Casts composed exclusively of fatty sub- 
stance are less common and suggest renal disease of a chronic 
type ; yet it does not follow that the kidneys always show a similar 
change at postmortem. The urine of phthisis and of chronic 
nephritis not infrequently con- 
tains fatty casts, wliich when 
composed largely of fatty mat- 
ter are highly refractive, short, 
with rounded ends, and rather 
irregular margins, while their 
surfaces are studded with oil- 
droplets. Fatty casts at times 
contain epithelial cells. 

Distinctive Features. — 
Fatty casts are readily distin- 
guished by allowing a drop of 
Sudan III (70 per cent, al- 
cohol saturated) or a drop of 
osmic acid to fall at the margin 
of the cover-glass, when the 
cover is so moved as to per- 
mit the stain to flow beneath it. The former of these preparations 
stains pink with fats; the latter, black. 

Amyloid Casts (Waxy Casts). — This form of cast is distin- 
guished by its large size and peculiar starch reaction. The casts 
are refractive bodies, often tape-worm-hke in outHne, broad, varying 
from a pale yellow to a yellowish-brown color, and their outline at 
times raised. Again this outline may be difficult of detection (Fig. 
119). Amyloid casts present a greater diameter than do other vari- 
eties, and are often of extreme length (Figs. 118, 119) ; yet specimens 
may be seen whose length does not exceed the diameter. On their 
surface are found leukocytes, erythrocytes, epithelial cells, crystals, 
droplets of oil, and granular debris. They may give amyloid reac- 
tion when treated with iodopotassic iodid or with methylene- 
19 




Fig. 117. — Urine containing pus, pus-casts, 
and epithelia (obj. B. and L. one-sixth). Patient 
an aged woman. 



290 



THE URIXE. 



\iolet solution, which changes amyloid substances to a blue or a 
mahogany color respectively; yet this reaction may be absent when 
the kidneys are amyloid, and present in casts where no such 
changes are found in the kidneys at postmortem. The exact 
composition of amyloid casts remains moot. 

Clinical Significance. — The presence of hyahne casts in the 
urine is diagnostic of chronic inflammator}' changes in the kidneys, 
although they may occur in acute nephritis, phthisis, amyloid 
disease, and in septic processes, of both acute and chronic nature. 
The darker variety of casts I have found in the urine of puerperal 
sepsis and of sepsis following operations. The paler forms have 




Fig. iiS. — Showing epithe'iai and amy- 
loid casts. Patient a femaie, aged forty- 
two years, suttering from septicopyemia 
with amyloid kidney (obj. Queen one- 
sixth; eye-piece 2;. 



Fig. iiQ. — Large amyloid cast containing' 
three renal epithelial cells upon its surface. 
Two short hyaline casts ; cluster of renal 
epithelium ; and few leukocytes (obj. B. and L. 
one-sixth). 



been observed (Plate 19) in the urine of puerperal eclampsia. "^ 
They are also a feature of chronic nephritis. 

Cylindroids. — These bodies were detected in the urine from 
scarlet-fever patients by Thomas. f They appear as ribbon-like 
bodies, rather lusterless, and drawn to a fine point at one extremity 
(Fig. 120). Their surface is commonly free from granular debris, 
but may show fine fines extending parallel to their lateral borders, 
as well as transverse elevations giring to the cyfindroid the 
appearance of a twisted tape. 

Clinical Significance. — Cyfindroids are found in the urine 
of persons suft'ering from renal congestion, nephritis, pyefitis, and 
cystitis. They may be found in urine containing an excess of 

* "Phila. Med. Jour.," Dec. 15, 1900. 

t " -\rch. f. Heiikunde," 1870, vol. xi, p. 130. 



CASTS (tube-casts; renal casts). 



291 



amorphous urates when the urate granules congregate upon the 
cylindroids, thus forming the so-called "urate casts" (Fig. 112); 
a feature of the urine in childhood, early adult life, and during con- 
valescence from acute fevers. In non-albuminous and otherwise 
healthy urines cylindroids may be found, and are therefore not 
diagnostic of renal disease. 

Floaters {Clap Shreds). — Congestion situated at any portion 
of the genito-urinary tract, preferably the urethra and adjacent 
structures, may cause the urine of such persons to contain small 
particles, or bodies, which are thrown down with the general sedi- 
ment, or which, at other times, remain suspended in the liquid at 
different distances from its surface. The composition of floaters 
varies within wide hmits. Guyon* distinguishes three varieties: 
(i) Those found at the top of the urine, composed of epithelium 
and mucus; (2) where a moderate 
amount of pus is added they sink some 
distance beneath the surface; and (3) 
where a preponderous amount of pus 
enters into their composition they sink 
to the bottom of the urine. 

Spermatozoa. — These cells are to 
be found in the urine of men suffering 
from pathologic spermatorrhea, after 
intercourse, or emission the result of 
other excitants, and in the urine of 
women after coitus. When seen in the 
urine, they are found to retain their 
normal outline but are not motile, and 
in old urines the tails are detached 
from the heads. They stain readily 

with a solution of carbolfuchsin, and should be thus studied 
when question arises as to their general properties (see Sperma- 
tozoa^ page 478). 

Fragments of Tumors. — Small polypi from the bladder- wall 
are occasionally observed in the urine, while particles from slough- 
ing surfaces, as of cancer, tuberculosis, or sarcoma of the bladder, 
furnish valuable aid to diagnosis. Malignancy of such structures 
as the vagina, rectum, and uterus may form fistulous communica- 
tion with the urinary tract, and discharge their products with 
the urine. The diagnosis of renal tumor from the study of 
urine is difficult, and should not be made unless other conditions 
present warrant such conclusions by the surgeon. Cancer frag- 
ments are frequently derived from a leukorrheal discharge which 

*"N. Y. Med. Jour.," July 14, 1900. 




Fig. 120.— Cylindroids : a, b. 
Cast-like forms ; c, filamentous 
forms (Ogden). 



292 THE URINE. 

has been added to the urine. Actinomycosis of the bladder is at 
times placarded by the appearance of the fungus in the urine 
(Fig. 121). 

Methods of Study. — Particles of tissue are best studied by 
teasing them with a fine needle, since they are usually too small 
for sectioning. In a case studied at the Philadelphia Hospital * 




Fig. 121. — Portions of a villous growth of the bladder: a, Magnified 190 diameters ; b, magni- 
fied 370 diameters (Ogden). 



the urine contained pieces of laminated membrane, scolices (heads 
of parasite), and booklets — the products from a hydatid cyst (Figs. 
122-125). 

ANIMAL PARASITES. 

Taenia Echinococcus. — This parasite rarely affects the urin- 
ary tract, yet its cysts may develop there and later discharge 
their contents with the urine. When the cyst is located in 

* " Amer. Med.," Jan., 1903, p. 20 



ANIMAL PARASITES. 



293 




Fig. 122.— I, Shreds of membrane; 2, cluster of scolices ; 3, scolex of Taenia echinococcus 
(obj. Queen two-thirds, eye-piece 4). 




Fig. 123. — Scolices and booklets, Taenia echinococcus, from urinarj' sediments (obj. Queen 
one-sixth, eye-piece 4). 



294 



THE URINE. 



the kidney's substance and communicates with the urinary tract, 

booklets and scoHces of the parasite in connection with shreds 

of the cyst membrane may be 
found in the urine, and in addi- 
tion to these findings the urine 
commonly contains blood and 
casts, as was personally noted 
in a case studied in 1897 at the 
Philadelphia Hospital (Figs. 122- 
125). Cysts inyohdng other \ds- 
cera may form fistulous com- 
munications with the urinary 
tract, in which instance the 
usual products of the cyst ap- 
pear in the urine. 

Filaria Sanguinis Hominis. 
— This parasite may appear in 
the urine of persons suffering 
from chyluria, or from hematuria 

of filarial origin. A similar case was studied by F. P. Henry. 

By way of repetition I studied the urine of an adult which 




Fig. 124.— I, Scolex of Tsenia echinococ- 
cus, showing crown of booklets ; 2, scolex 
and detached booklets (obj. B. and L. 
one-sixth). 




Fig. 125.— Urinary sediment showing blood- casts and booklets of Tsenia echinococcus (obj. 

Spencer one-sixth). 



showed hematoidin crystals and a parasite (Plate 17) of question- 
able classification. A surgeon removed one kidney from this 



ANIMAL PARASITES. 



295 



patient and reports that the pelvis and part of the kidney sub- 
stance were occupied by a colossal abscess filled with creamy 
pus. The filaria is quite as easy of recognition when in the 
urine as when found in the blood, and presents all its character- 
istics, except that it is non-motile or its movements greatly 
lessened. Urine containing filaria may show blood, chyle, or 
pus, and for this reason it is often regarded as the etiologic 
factor in certain forms of tropic hematuria (Fig. 49). Blood 
falls to the bottom of the urine. 

Schistosoma (Distoma) Haematobium. — The ova of this 
parasite are found in the urine of persons suffering from tropic 
hematuria, and were first described by Bilharz in 1851, who re- 




Fig. 126. — Schistosoma haematobium: i, Ova in blood-clots from urine (obj. Spencer two-thirds, 
eyepiece 4). 2, Ovum shown under one-sixth objective. 



garded them as an etiologic factor in the hematuria of Egypt. 
Harley, Brock, and others have studied this disease in the Cape 
of Good Hope and in the South African Islands, where epidemic 
hematuria is common. 

Urine containing these ova is apt to display a heavy sediment, 
which when studied under a low-power (two-thirds) objective is 
found to be composed largely of blood-clots, and it is in these clots 
that the eggs are found most abundant (Fig. 126). At times it 
is necessary to tease the clot in order to Hberate the ova from the 
mass; and after such treatment one often finds ova floating in the 
urine. To preserve these ova as permanent specimens the usual 



296 THE URINE. 

method employed for urinary sediments will be found of value 
(see Mounting oj Casts, page 259). 

The fully matured ovum is the shape of a hen's egg, j^j to yi-g- 
inch in length, and about ^^r ^^ 3T0 ^^ ^^ ^^^^^ ^^ breadth. An 
irregularity in size obtains even in mature specimens; some eggs 
being found narrow and long, while others are distinctly oval. 
The most immature ovum presents a hyaline envelop with a short 
spine (Plate 19A), and by careful focus is seen to contain granules 
of various sizes. Older specimens show segmentation in different 
stages, and by close study of such ova one may trace the various 
developmental stages, step by step, from a mere granular mass 
until the embryo attains a definite structure (Plate 19A). The cap- 
sule is sufficiently transparent to permit the study of its contents. 
At the narrow end it is continued as a short, sharp spine which has 
an average length of 2"wo" inch. 

"The embryo, until the time draws near for its obtaining liberty, 
lies quiescent in the shell, only now and then moving its head from 
side to side, or occasionally drawing its whole body upward with a 
jerking movement" (Brock).* The cephalic and caudal extrem- 
ities of the embryo are readily distinguished when under a one- 
sixth objective, the former being commonly directed toward the 
spine. Later the body of the embryo appears to be surrounded 
by cilia. The time required for the hatching of these embryos 
after they are voided vidth the urine varies from a few hours to 
several days. The capsule becomes thin and develops a longitu- 
dinal sHt through w^hich the embryo escapes (Plate 19A). When 
the urine above the sediment has been decanted and replaced by 
water, the embryos are to be seen swimming actively in this liquid 
(Brock). Through the courtesy of Dr. Claude A. Smith, of 
Atlanta, I was provided with urine containing many of these ova 
and was able to confirm the observations of Brock, as shown by 
the accompanying illustrations. The empty capsule is to be 
found floating in the liquid after the escape of its embryo. 

The further development of the embryo outside of the body 
and its mode of re-entering the system are not fully determined. 
The fact that bilharzia affects mostly males before the age of 
eighteen, a time when they bathe frequently in the streams of in- 
fected districts, as well as the additional evidence that women and 
girls of these districts are rarely known to bathe in the streams 
and are practically free from Bilharz disease, offers evidence favor- 
ing the parasites gaining access to the body during the act of bath- 
ing. It is possible that they may ascend the urethra, for it is to be 
remembered that the mature worm finds a resting-place in the 

* "Jour, of Path, and Bact.," Edinburgh and London, Oct., 1893. 



PLATE 19 A. 







H, '/ 



Uv'ji'\ 



~> 



)/ 



Schistosoma H^matobium. 

1-4, Various stages in development of embryo; 5, empty shell; 6, surviving em- 
bryo (after Brock); 7, ova in urinary sediment (personal observation). 



ANIMAL PARASITES. 297 

venous systems of the bladder or abdominal viscera, and her ova 
may escape with the urine, the feces, or the sputum. 

Oxyuris Vermicularis. — This parasite may in rare instances 
appear in the urine, either as a result of abnormal communication 
between the urinary tract and the rectum, or in the case of children, 
where the parasite enters the vagina or the urethra, in which in- 
stance the symptoms of acute inflammation of these parts are 
noted (see Vaginitis, page 484). In one case of vaginitis I found 
the urine to contain many ova and two specimens (females) of 
the oxyuris. 

Ascaris Lmnbricoides. — The ascarides or their ova are seldom 
found in the urine, and occur only as the result of fistulous com- 
munication between the rectum and the urinary tract. 

Rhabditis Genitalis. — The name given by Scheiber to a 
variety of worms which he found in the urine, believing the affec- 
tion to originate from the genito-urinary tract. I have observed 
the following described parasite in two cases of hematuria* seen 
at the Pennsylvania and Philadelphia Hospitals respectively. 
Dr. Ch. Wardell Stiles, of the Bureau of Animal Industry, at 
Washington, decHned to make a specific determination of this 
parasite. The patient, a male of sixty-one years, presented noth- 
ing abnormal for one of his age, and gave no history of having 
ever before voided bloody urine. On rising in the morning he 
noticed that his urine resembled blood, and it remained unchanged 
during the day. He suffered no discomfort, and during the day 
did not void urine oftener than usual. A specimen taken from 
that passed on retiring and during the night following was also 
bloody and contained a few parasites. In the morning the urine 
was normal in appearance, did not contain parasites, and the cen- 
trifugated sediment showed but few blood discs. The urine, on 
standing, displayed a heavy sediment, a microscopic study of which 
shov/ed it to be composed, for the most part, of blood-cells, clots, 
few epithelial cells, and many blood-casts. Everywhere the sedi- 
ment was found to contain many small worms, which are best 
described by the accompanying illustration (Fig. 127). A drop of 
this sediment, when studied under a two-thirds lens, often pre- 
sented from two to six of these parasites in a single field of the 
microscope. Their movements consisted in coiling and uncoiHng, 
apparently reaching forward with their tapering extremity — these 
movements being repeated in such rapid succession that they were 
enabled to travel across the field of the microscope in a few 
seconds. The serpentine movement, as shown by the embryos of 
the filaria, was not observed. They remained aHve for twenty- 

* "Amer. Med.," Jan. 3, 1903, p. 20. 



298 



THE URINE. 



four hours in a specimen of urine that had been placed in an incu- 
bator at a temperature of 37° C; but when kept at room tempera- 
ture they were found motionless after a few hours. In the urine 
there appeared to be great variation in the size of these worms, as 
is shown by the following measurements: Total length, 0.036 
to 0.053 inch; diameter at greatest part, 0.003 to 0.0035 inch; 
diameter at the junction of the greater one-fourth with the re- 
maining three-fourths of the body, 0.002 to 0.0025 inch. 

During my term of ser\ice at the Pennsylvania Hospital (1901) 
I studied a specimen of bloody urine, voided by a male patient, in 




Fig. 127. — Parasites found in bloody urine fobj. B. and L. one-sixth). 



which many parasites apparently identical with those observed 
in connection with the pre\ious case were found. 

Trichocephalus Dispar. — Ova of the Trichocephalus dispar 
were present in the urine of both patients (Fig. 171). 

Anguillula Aceti. — Few instances are recorded where the 
urine has contained this parasite, and while its detection is most 
unusual, it is necessary that every microscopist be ever alert con- 
cerning the A. aceti or "vinegar eel." The A. aceti (Plate 20) 
thrives in both alkaline and acid urines. The average size of the 
parasite is 1.2 mm. by 0.033 mm. ; while that of the female is about 
1.9 mm. by 0.06 mm., and few specimens are seen to reach 2.25 
mm. in length. The uterus of the mature female is distinct and 
contains two or more ova and less often embryos. The young 



PLATE 20. 




Vinegar Eel (Anguillula Aceti). 

1. Lateral view of male specimen of the vinegar eel {Anguillula aceti) from the 
human bladder (greatly enlarged). 

2. Caudal portion of same species: i, Intestine; /, testicle; sp, spicule; ap, 
accessory piece (greatly enlarged). 

3. Ventral view of cloacal opening of same, showing partially extruded spicules 
(greatly enlarged) . 

4. Outline lateral view of partially extruded spicules (greatly enlarged). 

5. Gravid female vinegar eel from the human bladder. Embryos and eggs 
are present only in the anterior horn of the uterus (greatly enlarged). 

6. Young embryos of same (greatly enlarged). 

7. 8. Somewhat older embryos (greatly enlarged). The esophagus is evident 
in both specimens (Stiles). 



ANIMAL PARASITES. 299 

forms may vary in length from 0.25 to 0.7 mm. The male worm 
is provided with a pair of thick, double, curved spicules on the 
ventral surface (Plate 20, Fig. 3), and projecting from each is a 
fan-shaped piece of fin. I have studied the urine from two pa- 
tients, one a male, in which the vinegar eel was present. The 
woman had been taking vaginal douches containing vinegar. 

Detection. — It is easy to obtain this parasite from table 
vinegar and thus conduct comparative studies. It resembles 
closely the Strongyloides intestinalis (see page 419), which is 
found in the feces, Thayer* having reported two American cases. 

Stiles has offered the following— 

KEY TO CLINICAL DIAGNOSIS OF WORMS IN THE URINE AND 
IN THE VAGINA. 

Eggs. 

1. Eggshell thick, ellipsoid, 64 to 68 // by 40 to 49 fJ., with mosaic structure; 

embryo not developed; indicates infection of kidney. . .Dioctophyme renale. 

Eggshell ovoid, 135 to 160 // by 55 to 66 /i, without mosaic structure, usually 
with sharp spine; contains ciliated embryo; indicates infection of blood- 
vessels with trematodes (Egyptian hematuria, bilharziosis) 

Schistosoma hcematobium, page 295. 

Eggshell thin, oblong, 50 to 54 /^ by 20 to 27 /u, contains elongated worm; 
indicates infection of rectum with pinworms not found in the urine of male 
patients Oxyuris vermicularis , page 414. 

Embryos. 

2. Embryo ciliated (bilharziosis) Schistosoma haematobium, page 295. 

Embryo not ciliated elongate 3 

3. Esophagus distinct, with posterior bulb armed with chitinous teeth (rhabditi- 

form embryos) 4 

Esophagus not very distinct, no posterior bulb; same embryos also found in 
the blood, 270 to 300 // long Filar ia sanguinis hominis, page 147. 

4. Embryo 140 ,u long; adults 3 to 12 mm. long in rectum 

Oxyuris vermicularis. 
Adults in urine, but not in rectum 8 

Larv^ and Adults. 

5. Elongated and flat; tape-worm larvae Sparganun Mansoni. 

Body round 6 

■6. Body large, may attain 40 to 100 cm. in length; usually red in color 

Dioctophyme renale. 

Body less than 12 mm. long, whitish 7 

7. Body 3 to 12 mm. long; male with single spicule; same parasite found in 

rectum Oxyuris vermicularis. 

Body less than 3 mm. long; male with two spicules and accessory piece 9 

8.- Male without caudal bursa Anguillula aceti. 

Male with caudal bursa Rhahditis pellio. 

Eustrongylus Gigas. — Evidence of this parasite is at times 
manifest in the urine and may be accompanied by chyluria or 
hematuria, Moscato recording a case of the former, and Clark one 
of the latter. Dr. John A. McKenna, of Philadelphia, has de- 

*"Jour. of Exp. Med.," Nov. 29, 1901. 



300 THE URINE. 

tected the ova of this parasite in the bloody urines of two children. 
Portions of the adult worm wxre obtained from one case in urine 
drawn by catheter. 

Bothriocephalus Liguloides. — Leuckart has recorded an 
instance occurring in eastern Asia where this parasite was found 
in the urine of man. 

Amoeba Urogenitalis. — Baelz * described under this caption 
large, actively motile amebas found in the urine and vaginal secre- 
tion' of a female aged twenty-three years, who was at that time suf- 
fering from pulmonary tuberculosis. 

Infusoria. — Urine may be found to contain these bodies when 
it has been allowed to stand for a time and is faintly alkaline in 
reaction. They have no known pathologic significance. The Trich- 
omonas vaginalis (Fig. 146) has been detected in the urine by 
Marchand, Muira, and Dock.f The author has studied bodies 
in the urine closely resembling the cercomonads found in the 
feces. 

VEGETABLE PARASITES. 

Fungi. — Normal urine when voided contains neither fungi nor 
bacteria in appreciable numbers, but when allowed to stand in a 
warm place these organisms soon develop (ten to twenty-four 
hours). They may be divided into molds, yeasts, fission- fungi, 
and bacteria, of which we find for the most part non-pathogenic 
forms. Urine undergoing ammoniacal change presents fission- 
fungi in great numbers and occasionally yeasts. ]\Iolds are not 
unusual when the urine contains sugar; but where alcohoHc fer- 
mentation has ceased this fungus develops with rapidity. Molds 
may form a thick surface growth which at first floats, but later 
may sink to the bottom of the liquid. Such urine is commonly 
turbid and in addition contains yeasts and numerous bacteria. 

Clinical Significance. — A copious growth of the yeast fungus 
in the urine is highly suggestive of glycosuria. 

Microscopically, decomposing healthy urine presents a variety 
of pictures ; and these changes are doubtless produced by a number 
of organisms, among which micrococci are given a prominent place, 
appearing on the surface in pure cultures (Micrococcus urea). 
This coccus is of large size and often forms in short chains. Ba- 
cilh of variable size, some containing spores, others in clusters and 
chains, of both motile and non-motile varieties, are also present 
in such sediments, together with cocci of various sizes, arranged 
singly, in pairs, and in clusters. Sarcinse of small size are occa- 
sionally met with in such urines (Fig. 138), and I have found 

* "Berl. klin. Woch.," 1883, vol. xxiii. 
t "Amer. Jour. Med. Sci.," Jan., 1896. 



PLATE 21, 






'<t. -?^-^^' 





Aspergillus. 

1. From cultures of aspergillus fumigatus on acid urine (obj. Queen one- 
sixth; eye-piece 2). 

2. Peculiar arrangement (octopus formation) of fungous growth. At lower left 
quadrant is a portion of the fungus (highly magnified). 

3. From urine during an attack of cystitis (obj. Queen one-sixth; eye-piece 2). 

4. From urine (diabetic) during an attack of cystitis (obj. Queen one-sixth; 
eye-piece 2). 

5. Aspergillus niger from culture on acid (diabetic) urine (obj. Queen one- 
sixth; eye-piece 2). 



VEGETABLE PARASITES. 30I 

them in the sediment of fresh urines prior to the development of 
fermentation. 

Actinomyces. — Actinomycosis is a rare disease of the genito- 
urinary tract, but where involvement of these organs exists, it is 
likely to be placarded by the appearance of the ray fungus or its 
products (mycelia) in the urine (Fig. 183). 

Aspergillus. — Renon observed spores of the Aspergillus fumi- 
gatus in the urine of animals suffering from experimental aspergil- 
losis.* The author has found both spores and myceha of the 
Aspergillus fumigatus present in the urine of acute cystitis, and in 
cystitis occurring in a diabetic (Plate 21); and has conducted a 
series of cultures studying the effect of both the A. niger and A. 
fumigatus on urines, f 

Bacteriuria. — A urine containing many bacteria when voided 
is to be regarded as a serious symptom even though the indi- 
vidual organisms present are not classed as pathogenic in nature ; 
yet such a condition of the urine may persist over a long 
period without other appreciable evidence of disease (idiopathic 
bacteriuria). Theoretically, bacteriuria should always ensue as a 
result of bacteremia. The urine contains specific bacteria during 
the course of certain infectious maladies. 

Method of Obtaining Urine. — Urine for bacteriologic study 
must be collected under aseptic precautions lest the result 
of our study be absolutely nil. To obtain urine from the female 
bladder, cleanse the vestibule of the vagina and mouth of the 
urethra by using first a solution of mercuric bichlorid (i : 1000) 
followed by a solution of boric acid and later by sterile water. 
Second, a glass catheter that has been previously sterihzed by 
boihng, and placed in sterile water, is now lubricated with sterile 
oHve oil or glycerin and introduced through • the urethra into 
the bladder. Third, allow the urine to flow off through the 
catheter for a few seconds. Then permit it to flow into sterihzed 
test-tubes or into a sterile bottle, and cork with sterilized cotton. 

Caution. — Inchne the open tube while the urine is entering it 
to prevent air-borne bacteria from faUing into the tube. Cork the 
tube or the bottle with the cotton stopper before placing it in the 
vertical position. Cultures may be made from urines thus ob- 
tained, and in my experience it has been rare to find such specimens 
contaminated by extraneous organisms. 

The same necessary precaution should be observed in obtain- 
ing urine from the male bladder, using a metal or rubber catheter. 

*"Comptes Rendus des Seances et Memoiries de la Societe de Biologie," 
Feb. 9, 1895. 

t"Phila. Hosp. Rep.," 1900. 



302 THE URINE. 

It is my practice to force bichlorid-of-mercury solution (i : looo) 
through the rubber catheter and then to immerse it in this solu- 
tion of bichlorid for a short time, which renders the chances of 
contamination by the catheter infinitesimal. 

The collection of urine from the kidneys by catheterization 
of the ureters requires, in addition, the assistance of the surgeon, 
as do also methods of segregation. 

Making Cultures. — The making of cultures and identifying 
micro-organisms are those commonly in vogue, and for the latter 
of these the reader is referred to special works upon bacteriolog}^ 

1. Take three culture tubes containing about 20 cc. each of 
agar-agar and heat them (by standing in warm water) sufficiently 
to liquefy the medium. 

2. Label these tubes (a), {b), (c). 

3. Shake the urine well and add to tube (a) one loop (one drop) 
of urine, stirring with the platinum needle (Fig. 197) to mix it 
well through the medium and pour into a Petri dish. To tubes 
{b) and (c) add tw^o and four drops respectively, and proceed as in 
the case of (a). 

4. Place plates in a cool place until the medium has sohdified ; 
then place in an incubator (temperature, 37.5° C.) for from twenty- 
four to forty-eight hours. Cultures and smears should be made 
from such colonies of growth as may develop, transferring the 
cultures to several forms of medium. 

5. In case a bacteriologic study is made at stated intervals the 
number of colonies developing from tubes (a), (b), and (c) re- 
spectively should be counted, and in this way the degree of bac- 
teriuria estimated. 

It is also well to make several slant inoculations on agar-agar, 
LoefHer's blood-serum, and on bouillon-peptone solution, special 
media being necessary for the gonococcus, tubercle bacillus, and 
bacillus of influenza. 

Staining of Bacteria. — Fill two or more of the special tubes of 
the centrifuge with the urine and centrifugate for five minutes; 
then remove the tubes and lift the sediment thus collected into a 
pipet and transfer a small drop of it to the center of a clean slide 
which has been arranged in the sKde forceps (Fig. 186); spread 
to form a thin film, dry by gentle heat, and stain for two minutes 
with carbolfuchsin or 5 per cent, aqueous solution of methylene- 
blue. 

Caution. — Remove the stain by allowing a feeble current of 
water to fall upon one end of the slide and to flood gently over the 
specimen. 

The specimen may be dried over a low flame or in the air and 



VEGETABLE PARASITES. 303 

mounted in Canada balsam. Study by the direct method consists 
in adding a cover-glass to the stained sediment before drying. 
Much time and labor may be saved by adopting this latter 
method, and by it specimens may be satisfactorily viewed under 
a one- twelfth oil-immersion objective. The staining of the 
tubercle bacillus and of the gonococcus will be given in detail 
in conjunction with the study of sputum. and urethral pus respec- 
tively, and allusion will be made to some of the bacteria to be 
encountered in the urine. 

Tubercle Bacillus. — This organism is found in the urine 
when ulcerative or suppurative tuberculous lesions involve or 
communicate with the urinary channel. In this situation the bacilli 
are commonly found in clusters and often intimately associated 
with shreds of sloughed tissue (Plate 30) . Isolated bacilli are not 
common, yet such findings may occur in connection with miliary 
tuberculosis, with or without ulcerative lesions of the genito- urinary 
tract; and according to Frick and Walsh, tubercle bacilH are to be 
found in the urine of a large percentage of cases of pulmonary 
tuberculosis (see Staining of Urinary Sediment, page 258). Per- 
sonally, I have studied over 1000 specimens of urine for tubercle 
baciUi and have found this organism but three times, though other 
acid-fast bacilli have been common findings. It is necessary to 
differentiate between the tubercle bacillus and the smegma bacillus 
(see page 441). Detection of the tubercle bacillus in the 
urine by means of cultures may at times be necessary, but is 
scarcely practicable; a more practical method of diagnosis where 
the bacilli are not found and the cHnical features suggest strongly 
their presence, is to inoculate a guinea-pig or a rabbit with a few 
drops of the suspected urine into the chamber of the eye, into the 
peritoneal or the pleural sacs, or subcutaneously, in which case 
the animal will develop tubercular retinitis, peritonitis, or pleuritis 
respectively. There is no form of inoculation with the tubercle 
baciUus more virulent to guinea-pigs than when the bacilli are 
contained in the urine. 

Gonococcus. — Gonococci may be present in the urine during 
the course of gonorrheal urethritis, at which time the organism 
stains with the usual anilin dyes (see page 495). I have found 
it difficult to detect beyond question of doubt the gonococcus in 
urinary sediments; and the differential staining by means of Gram's 
solution has been unsatisfactory, since I have not been able to 
make a positive diagnosis of gonorrhea through a microscopic 
study of the urine alone. 

Caution. — The urine of women not infrequently contains a. 
diplococcus which, from its staining properties alone, is indistin- 



304 



THE URINE. 



guishable from the gonococcus, and the identity of this organism 
is impossible except where cultural studies are conducted. The 
urine may under certain conditions modify the growth of the 
bacteria, and experience has forced me to regard bacteriologic 
study of the urine as of limited value when in reference to the 
gonococcus. 

Ulcerative Endocarditis. — Here, too, the urine at times 
contains the specific bacterium acting as a causal factor in the pro- 
duction of the endocardial lesion. Such study is impracticable, 
since a study of the blood furnishes more conclusive evidence. 

Septicemia and Pyemia. — The urine in these conditions 




Fig. 12S. — Streptococcuria : case of a male of eighteen years; history of albuminuria 
for six months. Urine also contained few cylindroids and hyaline casts (obj. B. and L. one- 
twelfth oil-immersion). 



may rarely contain clumps of pathogenic cocci, and seldom these 
bodies are arranged in the form of casts which appear to be- formed 
of bacteria. It is to be borne in mind that at such times all vital 
structures are much reduced, thus forming a suitable soil for bac- 
terial developments along the urinary tract, and that these bac- 
teria, in part at least, may not enter the urine through the kidneys. 
Acute Nephritis. — Many writers have found cocci in the 
urine of this affection, and bacilli are reported as occurring in the 
nephritis of children ; but as yet their diagnostic value is restricted. 
In the acute nephritis complicating pneumonia, diplococci have 
been found. The theory of bacteriuria in the nephritis of acute 



VEGETABLE PARASITES. 305 

infectious fevers appears plausible and has been ably exemplified 
in a number of instances; e. g., typhoid fever. The accompany- 
ing illustration (Fig. 128) was made from the urine of a youth 
viio was suffering from subacute nephritis. 

Typhoid Fever. — Typhoid bacilh are described as occurring 
in the urine of persons suffering from this disease by Nevv^mann,* 
who found the organism present in six of twenty-three cases studied. 
Wright and Semple found typhoid bacilh in six of seven cases 
studied. t Gwynn has made an exhaustive study of the subject,! 
from which he concludes that typhoid bacilh appear in the 
urine of typhoid patients in 30 per cent, of the cases ; and since this 
report there have followed a number of reports, most of which have 
been confirmatory of Gwynn's observations, few finding these ba- 
cilh present in a higher percent- 
age of cases. 

Clinical Sign ificance. — Typhoid 
bacilH may occur early in the 
course of the disease, but are more 
commonly present by the third 
week; they persist during conva- 
lescence and often for a long time 
thereafter, and are present in the 
urine of both severe and mild 
cases of enteric fever. Urine con- 
taining typhoid bacilh displays a 
fine clouding which lends a hsfht „. ^ ..,,.,,. . 

C) c3 Fig. 129.— Typhoid bacilh in urine. 

and finely flocculent appearance Third week of 'disease stained with 

-l . rr^i • 1 carbolfuchsin (obj. B. and L. one-twelfth 

to the iresh specimen, ihis, now- oil immersion). 
ever, is not constant, and the urine 

may present the usual febrile characteristics where many ba- 
cilh are present (cloudy, dark color, and a heavy sediment). 
Cultures are often pure, and smears made from the urine's sedi- 
ment show many bacilh (Fig. 129). Richardson concludes that 
the percentage of cases in which typhoid bacilh appear in the 
urine bears a somewhat similar relation to the percentage of cases 
where the bacilh are present in the blood. The presence of 
typhoid bacilh in the urine may be influenced greatly by the 
administration of certain drugs, as urotropin, and by local treatment 
directed to the bladder. Their presence bears no relation to the 
severity of the disease, and is not influenced by the presence of 

* "Berl. klin. Woch.," iS88. vol. xxv, Nos. 7 and 9. 
t "Lancet," July 27, 1895. 

j "Johns Hopkins Hosp. Bui.," June 18, 1899 ; Phila. Co. Med. Soc, Oct. 24, 
1900. 




3o6 THE URINE. 

complications or sequelae. The presence of large numbers of 
these bacilli is suggestive of the disease in the absence of other 
valuable symptoms and signs. 

Identity. — Where these bacilli are found to decolorize by Gram's 
method of staining, and to present the morphologic characteris- 
tics, as well as the peculiar agglutination reaction with the patient's 
serum (Widal reaction), it will be safe to determine the presence 
of typhoid bacilh in the urine in typical cases. 

Reaction. — Such urine commonly gives an acid reaction when 
voided, and may even remain acid after standing for a long time. 
The number of bacilli present in the urine varies greatly. 

Erysipelas. — In this disease, where comphcated by acute 
nephritis, the urine has been found to contain organisms indis- 
tinguishable in form from the Streptococcus pyogenes erysipe- 
latis of Fehleisen. In the study of a large series of cases at 
the Philadelphia Hospital (54 in all) I was unable to recover such 
streptococci from the urine, though a few of these urines contained 
a trace of albumin. Non-pathogenic streptococci were present in 
some of the specimens. 

Glanders. — In 1885 Philipowicx "^ detected the bacillus of 
glanders in the urine of a man suffering from this disease. 

Relapsing Fever. — The spirillum found in the blood during 
the paroxysms of this disease appears in the urine when hematuria 
obtains, and during the febrile exacerbations the urine has been 
found to contain many bacteria. 

Colon Bacillus. — This organism (bacilH members of the 
colon group) is normally present in the urethra, and becomes 
numerous in the urine in cases of urethral and of vesical congestion, 
urethral stricture, prostatitis, and during- constipation (see Acute 
and Chronic Cystitis and Pyelitis). The bacillus of Sternberg 
and other members of this group have been recovered from the 
urine of yellow fever, but their presence has not been shown to be 
of chnical significance. 

Diphtheria. — The Klebs-Loeffler bacillus occurs in the urine 
when the diphtheric lesion is situated so as to communicate with 
some portion of the genito-urinary tract; and since this bacillus 
enters the circulation in malignant types of infection (see page 459) 
its recovery from the urine in such instances is to be anticipated. 

Scarlet Fever. — Here, also, the urine may contain many 
microorganisms; as streptococci, bacilli, diplococci, and micro- 
cocci. I have found it difficult to show any relation existing 
between such organisms and the disease in question. Class has 
found the "Diplococcus scarlatinas" in pure cultures in the kid- 

* " Wien. med. Blat.," vol. xxxiv, pp. 673 and 710. 



VEGETABLE PARASITES. 307 

ney's substance of animals inoculated with this organism,* and has 
also cultivated this diplococcus from the urine of persons suffer- 
ing from scarlet fever who presented scarlatinal nephritis. 

Acute Cystitis. — The reaction of the urine will be found 
to vary according to the bacterium present. Probably 50 per cent. 
of cystitic urines will show infection with the Bacillus coh communis 
(commonly in pure cultures) and the degree of acidity high; while 
in a staphylococcous infection the acidity is not decided. The 
Staphylococcus pyogenes albus occurs in from 15 to 25 per cent, 
of cases, and far less often the Staphylococcus pyogenes aureus is 
found. The Bacillus pyocyaneus when present is placarded by 
the greenish tinge it lends to the urine, which color (green) in- 
creases if the urine is kept at incubating temperature. T. R. 
Brown t reports a case of infection with this organism, and I have 
found it in the urine of acute cystitis twice; once in pure cultures. 

The Bacillus proteus vulgaris has been found by Brown in 
alkaline (ammoniacal) urines containing both blood and pus. 

Chronic Cystitis. — In the study of 24 cases Brown | re- 
covered from the urine Bacillus coli communis eleven times, and 
once the Bacillus tuberculosis; Staphylococcus pyogenes aureus 
three times; Staphylococcus pyogenes albus twice; and in two 
cases pyuria existed with sterile urine. In seven cases of cystitis 
with pyehtis the Bacillus coli communis was recovered four times 
(urine acid) ; Bacillus proteus vulgaris once, and Staphylococcus 
albus twice (alkahne or acid alternating). 

Acute and Chronic Pyelitis. — In nearly 50 per cent, of 
cases in which urine is obtained by catheterization of the ureters 
the colon bacillus will be found, in which instances the urine 
is acid. The Bacillus proteus vulgaris figures in from 20 to 30 per 
cent, of cases (alkahne urine). Where the process is tuberculous, 
the Bacillus tuberculosis is to be found by staining and by inocu- 
lation of animals with the suspected urine. Cultivation of this 
organism from the urine is impracticable. 

* "Proc. Path. Soc. Chi.," May, 1899. 

t" Johns Hopkins Hosp. Rep.," vol. x, Nos. 1,2. Xlhid., vol. x, Nos. i, 2. 



CHAPTER III. 
GASTRIC CONTENTS. 

The contents of the stomach is composed of the fluids secreted 
by the pyloric and by the cardiac glands of the stomach, which 
provide its active digestive ingredients; it also contains a portion 
of the buccal secretion which has gained access to the stomach 
through swallowing, but at the time when we recover the stomach- 
contents it is much altered, due to the digestive action of the fluids 
secreted by the stomach-glands. 

METHOD OF COLLECTION. 

The Stomach- tube. — The stomach-contents is best collected 
by the use of the stomach-tube, which is but a modifica- 
tion of the tube first devised and employed by the late Dr. 
PhiHp S. Physick, then Professor of Surgery in the University 
of Pennsylvania. Physick pubhshed a description of his original 
device in October, 1812, in the "Electrical Repertory," vol. iii, 
p. iii; but this instrument had been used by Dr. Physick since 
its first employment in 1800, when, so far as the records show, 
he first emptied the stomach of its contents by this method, and 
introduced into the stomach stimulants to patients from whom 
he had removed poisonous drugs. In 1803 Dr. Physick had 
made, in Paris, a special tube for the evacuation of the stomach. 
Julius Friedenwald* has pubhshed an interesting historic ^ note 
on this instrument. 

This tube should be at least 75 inches in length, and provided 
at one extremity with three fenestra: one at the end of the tube, 
the other two at its side, about one and two inches respectively 
from the tip. The other extremity of the tube is expanded into 
a funnel, the base of which is from three to four inches in diameter, 
and the portion of the tube between the funnel and the fenestra 
is of a constant cahber of about one-half inch in diameter. Many 
operators prefer a tube in sections anchoring the one extremity to 
a glass funnel. The accompanying cut (Fig. 130) will illustrate 
the tube with which I have had the most satisfactory results. 

* "Johns Hopkins Hosp, Bui.," Sept., 1903. 
308 



METHOD OF COLLECTION. 



309 



Boas has devised a special bulb, which is usually located midway 
between the portion of the tube showing the black circle and the 
funnel; but where the sole object is merely to evacuate the stomach, 
I have found this bulb of no service. In fact, a tube with an 
expanded portion between the funnel and the fenestra is often 
most annoying, and I have never found this expansion of any 
practical value. The foregoing statements are not to be confused 
with the employment of the stomach-tube for the ascertainment 
of the. capacity of the stomach or for the purpose of distending 
this viscus and thus outlining its position; in the latter of which 
instances air must be forced into the stomach, but the technic 
for such procedure is not 
within the scope of this 
volume. 

Counterindicatio n s . — 
Among the counterindica- 
tions to the introduction of 
a tube into the stomach 
are : Valvular heart disease 
where compensation has 
been lost; thoracic aneu- 
rysm; angina pectoris; pul- 
monary or gastric hemor- 
rhage; severe bronchitis; 
arteriosclerosis of high 
grade; and the various 
febrile diseases, including 
pulmonary tuberculosis. 

The introduction of a tube Fig. 130.— stomach-tube: ^, Fenestra near tube's 

• , , 1 ., 1 • . 1 • end ; B, funnel-like expansion ; C, mark showing: 

mtO the stomach m this distance to be introduced. 

latter condition is attended 

with a certain amount of risk, due to the fact that tuberculous 
ulceration of the stomach, while. rare, may exist and the organ 
be perforated. Perforation results from extreme retching, rather 
than from the instrument itself. In one such case I have seen 
rupture of the stomach occur, and I can recall two instances where 
the stomach-tube was passed directly into an aneurysm. 

Introduction. — i. Place the tube in a bowl containing warm 
v/ater; elevate its funnel end at a distance of about two feet 
above the bowl, and pour through the tube at least one pint 
of warm water; then allow the entire tube to remain coiled in 
the bowl of warm water. 

2. In case the patient is not confined to bed, direct that all 
clothing around the chest and abdomen be loosened so that the 




3IO 



GASTRIC CONTENTS. 



epigastrium is covered by a single layer of clothing composed 
of a thin garment. The patient is now directed to sit comfort- 
ably in a chair or to be pillowed up in bed; where there is some 
objection to the patient sitting, direction should then be given 
to have him lie on his left side. Place a heavy towel over the 
patient's chest, and pin it at the back of the neck in order to 
prevent the saliva, which always flows freely from the mouth 
while the tube is in position, from soiHng the clothing or causing 
the patient discomfort. 

3. Most important in the introduction of the stomach-tube 




Fie 



;i. — Aspirator of Boas (one-half natural size). 



is it to obtain the patient's confidence and to assure him, without 
hesitancy, that the instrument will not harm him, and that the 
sHght smothering sensation and nauseating effect which it always 
excites are increased by his own effort; and that if he will try 
to control the spasm of his throat, you will be able to introduce 
the tube more easily, and that the choking sensation will be 
materially lessened. This step performed well, all difficulties 
are ended and the stomach-tube is introduced with comparative 
ease in the most hysteric persons; neglected, it is always intro- 
duced with difficulty. 



METHOD OF COLLECTION. 



311 



4. Remove the tube from the water, and without drying grasp 
it between the thumb, index-, and second fingers (Fig. 132). Direc- 
tion should be given to the patient to open the mouth and to lower 
the chin shghtly, when introduce about six inches of the tube, pass- 
ing it directly over the tongue to the back of the throat. The patient 
is now directed to swallow, and the tip of the tube will immediately 
enter the esophagus. Pass the tube gradually by the thumb and 




Fig. 132. — Position of the patient for introduction of stomach-tube ; also method of passing 

tube into the mouth. 



finger, taking care to exert force only at the time when the patient 
swallows — and he should be directed to swallow as often as possible. 
Continue this introduction until the circle-mark on the tube (Fig. 
130) reaches the patient's lips; then hold the tube in position by 
the left hand and drop the funnel into the receptacle for the fluid. 
At this point in the operation direct the patient to bend forward 
and to endeavor to contract and relax his abdominal muscles ; or 
to cough shghtly three or four times in succession. Should these 



312 



GASTRIC CONTENTS. 



efforts fail to expel the stomach-contents, the operator should place 
his left hand over the epigastrium and exert gentle pressure while 
the patient repeats the expulsive efforts previously described. 

In rare instances it is impossible to recover any fluid in this 
manner, when it is necessary to have a glass containing just 
sufficient water to fill the tube from its funnel to its tip. Elevate 




Fig. 133. — Method of inducing expulsion of gastric contents by siphonage, as directed in the 

text. 



the funnel and pour this quantity of water in it, and at the moment 
all the water enters the tube, the funnel is dropped into a clean 
bowl and the expulsive efforts repeated both by the patient and 
by the operator (Fig. 133) The water that was introduced into the 
funnel will be expelled, and is likely to be followed by a free flow of 
the gastric contents. In order to prevent the gastric fluid from being 
diluted with the water the funnel is placed in a second receptacle 



METHOD OF COLLECTION. 313 

as soon as the water has escaped; thus the gastric juice will be 
a correct representative of the stomach's secretion. After the 
gastric fluid has started to flow, it is not hkely to be checked, or 
at least to stop entirely, until the stomach is emptied of its Hquid 
substance. 

Difficulties. — The most common obstacle encountered is the 
clogging of the fenestra of the tube with particles of undigested 
food ; and whenever this occurs, the tube must needs be removed 
and again introduced, or the funnel of the tube elevated and a few 
ounces of water poured into it. In case the water dislodges the 
obstruction, the stomach-contents and water introduced may be 
removed without further annoyance; but such gastric fluid is 
of no value for chemic analysis. Should the tube be introduced 
merely for the purpose of removing mucus or chemicals, this 
process is to be recommended. 

Aspiration. — Rarely indeed will it be found necessary to 
employ aspiration, and for this purpose Boas' bulb-tube will be 
found serviceable (Fig. 131). While the stomach-tube is intro- 
duced, its proximal end is compressed and the bulb then com- 
pressed firmly; then clamp the distal end of this bulb, release the 
pressure at the proximal end, and permit the bulb to expand. 
Through this method a vacuum is created in the tube which 
favors the flow of gastric fluid. Another method which may 
be employed is to connect the tube with an aspirating bottle, such 
as is employed for the removal of exudates from the pleural 
cavities. I have not obtained satisfactory results with either of 
these methods, and am incHned to regard siphonic action as pref- 
erable. 

Washing the Stomach. — Where the stomach is washed out 
merely for the purpose of removing mucus or long-retained food 
or for its psychic effect upon the patient, the tube should be intro- 
duced as previously described, and its funnel held at a point about 
four inches above the level of the patient's mouth (greater ele- 
vation may induce gastric pain and is liable to excite violent spasm 
of the stomach). Then the funnel should be filled with warm 
water and the water allowed to flow gradually into the stomach. 
In this manner 500 to 1000 c.c. of fluid may be introduced, but 
in order that this quantity be taken, the expression of the patient 
must be w^atched carefully, and upon the slightest evidence of 
discomfort or of retching the tube should be clamped below the 
funnel and the flow discontinued for a few seconds, when, in 
the majority of instances, the introduction of the fluid may be 
continued without special annoyance to the patient. In order 
to remove this fluid direct the patient to lean forward and drop 



3^4 



GASTRIC CONTENTS. 



che funnel into a vessel standing at his feet. The fluid will flow 
into the vessel gradually without moving the tube, and the 
entire stomach-contents will be emptied. This washing may be 
repeated two, or even three, times at a single introduction of the 
tube. 

Removal of Poisons. — In attempting to remove poison from 
the stomach it is well to introduce as much warm water as 
possible before attempting to encourage the flow of the gastric 
contents. It is practically impossible, and always extremely 
difficult, to empty the stomach of its contents through the stomach- 
tube after a full meal; and when this is necessary, it is well first 
to induce vomiting either by the drinking of Hquids (warm mus- 
tard water) or by the administration of apo- 
morphin (J grain hypodermically). 

Removal of the Tube. — Grasp the tube at a 
point about three inches distant from the patient's 
mouth, and compress it firmly between the thumb 
and index-finger; then withdraw the tube grad- 
ually — do not release the pressure until the tube 
is returned into the jar in which it was placed 
immediately before its introduction. Where no 
fluid has been obtained from the stomach the tip 
of the tube is held over a receptacle and the 
pressure released in the hope that a small quantity 
of gastric fluid may have been contained in the 
tube and will in this way be recovered. 

Cleansing the Tube. — The tube may at times 
become plugged with a particle of food, and 
should it be impossible to dislodge this substance 
by elevating the funnel as high as possible and fiUing it with water, 
the funnel should be suddenly lowered to the other extreme, in 
the hope that the combined forces of siphonage and aid induced 
by the patient may accomphsh this end. Should it be impos- 
sible to dislodge the obstruction in this manner, remove the tube 
and compress it firmly between the thumb and index-finger, 
beginning at its tip and gradually extending toward the funnel; 
compression and moderate stretching of the tube will usually 
dislodge this substance. Rarely it is necessary to dislodge the 
obstructing particle of food by air-pressure, for which purpose 
Pohtzer's bag will be found of service. 

Einhorn's Instrument. — Einhorn advocates a most ingenious 
device (Fig. 134) for the purpose of recovering small quantities 
of fluid from the stomach in persons where there exist certain 
counterindications to the introduction of the stomach-tube. 




Einhorn's 



capsules. 



TEST-MEAL. 315 

This instrument consists of a silver, olive-shaped vessel, eleven- 
sixteenths of an inch long by five-sixteenths of an inch at its 
greatest width. The opening of this instrument is rather large, 
and immediately above it there is attached a silver thread i6 
inches in length. The instrument is sv^allowed for the w^hole 
length of the thread, and should it not pass for that distance, it 
is to be understood that the instrument has not yet reached the 
stomach. Allow the instrument to remain in the stomach for 
five minutes, when remove by gentle traction upon the silver 
thread. 

By this method it is usually possible to obtain sufficient gastric 
fluid for the purpose of testing for free hydrochloric acid, lactic 
acid, and possibly for the total acidity; yet it is apparent that but 
a Umited quantity of fluid can be obtained through the use of this 
instrument. 

TEST-MEAL. 

The secretion of gastric juice is continuous, but the quantity 
that we are able to obtain with the stomach-tube is usually small, 
except during the process of digestion, and for this reason it is 
preferable that the stomach-glands be stimulated to activity before 
attempting to collect the gastric fluid. The most efficient and 
practical method whereby we can accompKsh this end is through 
the administration of a test-meal; although glandular activity 
of the stomach is to be accompHshed by thermic and electric 
stimulation to this viscus. The test-meal, furthermore, gives 
an idea of the secretory, resorptive, motor, and digestive powers 
of the stomach. 

The results of chemic analysis of the gastric juice will be found 
to fluctuate greatly, depending upon the character of food admin- 
istered at the test-meal. It has been found that starches and fats 
stimulate gastric secretion but moderately, but that a profuse 
secretion follows the ingestion of proteids. The gastric fluid is 
influenced by the taking of fluids at the time of the test-meal, or 
immediately before the gastric contents is collected. Again, the 
height of digestion will be found to vary in time after the adminis- 
tration of a test-meal, this variation depending upon both the 
quantity and the character of the food ingested. The various 
investigators have endeavored, therefore, to recommend a test- 
meal of definite composition and volume, advising that the gastric 
contents be withdrawn at a certain time after the administration 
of this meal. I have deemed it profitable, therefore, to describe 
the following test-meals: 

Ewald-Boas' Test-breakfast.— The test-breakfast of Ewald 



3l6 GASTRIC CONTENTS. 

and Boas consists of 35 to 70 grams (2 oz.) of wheat bread and 
300 to 400 ex. (one and one-half to two glasses) of water. Weak 
tea without sugar may be substituted for the water. This meal 
should be administered early in the morning, when the stomach 
is emipty, and before any food or hquid has been taken. The plan 
which I have adopted is first to wash out the stomach thoroughly, 
taking careful note — (i) of the quantity of gas that escapes upon the 
introduction of the tube; and (2) of the mucus contained in the 
washing. The test-meal is now given, the patient being directed 
to eat the bread slowly and to sip the water while eating. 

Collect the gastric contents one hour after the test-meal has 
been ingested. 

RiegePs Test-dinner. — The test-dinner of Riegel consists 
of 400 c.c. (13.5 fl. oz.) of soup, 200 grams (7 oz.) of beef-steak, 50 
grams (1.7 oz.) of wheat bread, and 200 c.c. (one glass) of water. 

Collect the stomach-contents four hours after the meal has 
been given. 

Caution. — The steak given at this meal should be chopped 
finely, lest particles of meat obstruct the lumen of the stomach- 
tube. 

Boas' Test-breakfast. — Boas' test-breakfast consists of 
oatmeal soup (a teaspoonful of rolled oats in one liter of water, 
boiled down to 500 c.c. — 17 fl. oz.) and sufficient salt added to 
render the soup palatable. In this meal Boas' object was to 
obviate the introduction of lactic acid with the test-meal, and, by 
avoiding bread, which contains a certain amount of lactic acid, 
this end is accomplished. This test-breakfast is necessary only 
where it is desired to estimate the quantity of lactic acid present; 
and where this knowledge is required, it is well to wash the stomach 
thoroughly the night before the administration of the test-break- 
fast. 

Collect the gastric contents one hour after the meal has been 
taken. 

Salzer Test-meal. — The double test-meal of Salzer consists 
of a breakfast of 30 grams (i oz.) of lean, cold roast-beef, which is 
chopped sufficiently fine not to obstruct the lumen of the stomach- 
tube; milk, 250 c.c. (8 fl. oz.); rice, 50 grams (1.7 oz.); and a 
soft-boiled egg. Four hours later the Ewald-Boas test-breakfast 
is given. 

Collect the gastric contents one hour later — five hours after 
the administration of the first meal. 

Through this double test-meal the gastric juice is obtained at 
the height of digestion, and the stomach's power of motility is 
also appreciated, which motility under normal conditions is 



CHARACTERISTIC FEATURES OF THE GASTRIC JUICE. 317 

sufficient to have removed the first meal entirely. Whenever 
the gastric contents is found to contain particles of meat admin- 
istered with the first meal, the motor power of the stomach is 
diminished. 



CHARACTERISTIC FEATURES OF THE GASTRIC JUICE. 

The gastric juice, when pure, is an almost clear, faintly yellow 
Kquid, having a sour taste, a pecuhar odor, and a specific gravity 
varying between 1.002 and 1.003. The reaction of the gastric 
juice is acid, due to the presence of hydrochloric acid, and is 
found to contain about 0.5 per cent, of solids. 

Amount. — Bidder and Schmidt conclude that the gastric 
juice secreted during the twenty-four hours is equivalent to about 
one-tenth the body weight; while Beaumont estimates the quantity 
of gastric juice at 180 grams a day. There can be but little doubt 
that the quantity of gastric juice secreted varies widely both in 
health and in disease; and that such conditions as diet, exercise, 
general nutrition, and environment, as well as age, sex, and 
occupation, all influence materially the glandular activity of the 
stomach. Boas claims that from 20 to 50 c.c. (i fl. oz.) should 
be extracted from the stomach of a healthy individual one hour 
after the ingestion of Ewald's test-meal; and I have always found 
it possible to extract this quantity of fluid under similar condi- 
tions. It is usually possible to recover from i to 50 c.c. of fluids 
from a stomach during the non-digesting period. The quantity 
of fluid obtained after a test-meal is governed by the motor power 
of the stomach; the size of the stomach; the degree of transuda- 
tion ; the degree of resorption ; by the fluid ingested with the test- 
meal; the power of contraction of the stomach, and the activity 
of the gastric glands. 

Excess. — An excessive quantity of gastric juice is to be 
found in connection with a hypersecretion, and may occur only 
at certain periods, or in rare instances this may be constant. It 
is impossible to establish a diagnosis of hypersecretion except 
w^here the gastric fluid is withdrawn and carefully measured at 
various hours during the day, at which times from 100 to 1000 
c.c of pure gastric juice are to be obtained from the so-called 
non-digesting stomach. It is also well to empty the stomach 
before retiring, and again to insert the tube in the morning after 
a night's rest. In this way it is possible to recover an excess of 
gastric fluid during the course of certain pathologic conditions; 
but it is hardly probable that such fluids are always true gastric 
juice. 



3l8 GASTRIC CONTENTS. 



MOTOR POWER OF THE STOMACH. 

The motor power of the stomach should be such as would 
rid this viscus of all particles of food, or practically all solid 
particles, within a period of six hours after the administration of 
Riegel's test-meal. It should also be found empty in from one 
and one-half to one and three-fourth hours after the ingestion of 
Ewald's test-meal. 

Clinical Significance. — The food will be retained in the 
stomach for an abnormally long period wherever dilatation 
exists, such retention varying in time, dependent upon the degree 
and character of the dilatation. Where the dilatation is extreme, 
it is possible to recover from the stomach great quantities of food, 
some of which may have been eaten several days before. 

Food may be recovered from the stomach in from twelve to 
twenty-four hours after it has been taken in cases of acute gas- 
tritis, and less often is this so in subacute gastritis. The food 
may be retained in the stomach where a simple atony exists. 

Leube's Method. — The stomach is thoroughly emptied 
through the stomach-tube and then Riegel's test-meal adminis- 
tered. Six hours later reintroduce the stomach-tube and with- 
draw as much as possible of the stomach-contents ; then introduce 
about 300 c.c. (10.14 fl- oz.) of warm water through the tube; 
\sithdraw this quantity. Repeat this washing two or three times 
until no particles of food escape through the tube and the wash- 
water is clear. 

Should this washing contain only minute particles of food, 
the motor power of the stomach is normal. This method is highly 
practical on account of its ease of execution, and in my experience 
has given most satisfactory results. 

Ewald-Sievers' Method. — This method depends upon the 
fact that saiol is broken up into phenol and saHcylic acid when 
introduced into an alkaline medium; and that w^henever this 
change is effected, the saUcyHc acid is ehminated through the urine 
in the form of saHcyluric acid. The time at which the salol 
passes from the stomach (an acid medium) into the intestine (an 
alkaline medium) is, therefore, placarded by the appearance of 
salicyluric acid in the urine. 

A capsule containing i gram (15 gr.) of salol is administered 
after a full meal. Collect in separate bottles a portion of the 
patient's urine, voided one-half hour, one hour, one and one- 
half, two, twelve, and twenty-four hours later. These different 
specimens should all be tested for the presence of salicyluric acid : 
Place a few cubic centimeters of the filtered urine in a test-tube, 



RESORPTIVE POWER OF STOMACH. 319 

and to it add a small quantity of a solution of sesquichlorid of 
iron. Salicyluric acid causes a violet color with this reagent 
(see Urine, page 256). 

Clinical Significance. — After the introduction of the capsule 
of salol into a normal stomach a positive reaction is given with 
the urine voided from forty-five to seventy-five minutes later, 
and where the reaction is retarded, the motor power of the 
stomach is diminished. The specimen of urine obtained at 
the end of the twenty-four hours should, under normal con- 
ditions, give a negative result, showing that the salol had been 
ehminated prior to the secretion of this specimen. Where gastric 
dilatation exists, the urine may give a positive result after twenty- 
four hours. Failure to obtain a reaction for sahcyluric acid with 
any of the specimens collected during the twenty-four hours points 
to pyloric stenosis. 

Fallacies. — It is to be borne in mind that salol is rarely 
decomposed in the stomach through the agency of alkahne mucus, 
which expedites the reaction for sahcyluric acid. The intestinal 
fluid may be acid in reaction as a result of fermentative changes 
(acetic and butyric fermentation). This condition delays the 
reaction for sahcyluric acid. 



RESORPTIVE POWER OF THE STOMACH. 

The resorptive power of the stomach is best ascertained in the 
following manner: Just prior to the taking of a full meal a 
capsule containing 0.2 gram of potassium iodid is given. The 
saliva is now to be tested, at intervals of from two to four minutes, 
for the presence of potassium iodid, by strips of filter-paper wet 
with stock solution. When the resorptive power of the stomach 
is normal, the paper takes on a violet color in from seven to eleven 
minutes after the ingestion of the capsule; and in from seven and 
one-half to fifteen minutes a blue tint may also be found. 

Clinical Significance. — The resorptive power of the stomach 
is delayed in gastric dilatation and in carcinoma. A less marked 
retarding of the appearance of potassium iodid in the sahva is to 
be found in chronic gastritis, and, at times, where gastric ulcer 
exists. Exceptions to this rule are by no means uncommon. 



GUNZBURG'S METHOD FOR INDIRECTLY EXAMINING THE 
GASTRIC JUICE. 

Giinzburg suggested the following method for the indirect 
examination of gastric contents of persons wherein there existed 



320 GASTRIC CONTENTS. 

some counterindication to the use of the stomach-tube : Place a 
tablet containing 0.2 to 0.3 gram of potassium iodid in an extremely 
thin but well- vulcanized piece of rubber tubing, which, when the 
ends of the package are folded neatly, will vary from 2 to 2 J cm. 
in length. Around this tubing are tightly tied two or more threads 
of fibrin which have been previously treated with alcohol. Giinz- 
burg has advised that each package be placed in warm water for 
several hours before use, and that later this water be examined 
for the presence of potassium iodid. In the event of no iodid 
being present, the package is considered fit for use. The bands 
of fibrin are dissolved when brought in contact with free hydro- 
chloric acid, and their dissolution is indicated by the appearance 
of the potassium iodid in the sahva. 

The patient is previously prepared and given Ewald's test- 
breakfast (p. 315); forty-five minutes later he is permitted to 
swallow the packet containing the potassium iodid. Examine the 
saliva for the presence of potassium iodid at intervals of from 
twelve to fifteen minutes. It may at times be necessary to continue 
these examinations for a period of six hours before a positive 
reaction for iodid will be obtained. 

Clinical Significance. — When this packet is introduced into 
a normal stomach, the sahva should give a positive reaction for 
potassium iodid after a period of one to one and three-quarter 
hours has elapsed. When hyperchlorhydria is present, the re- 
action may be tardy, appearing in from two and one-half to four 
hours. A similar result is also witnessed when hypochlorhydria 
exists. When a positive reaction is not given by the sahva for a 
period of from five to six hours after the ingestion of the packet, 
anchlorhydria probably exists. 

Giinzburg's packets are prepared abroad, and for this reason 
have not come into common use in America. 



CHEMISTRY OF THE GASTRIC CONTENTS. 

The gastric juice consists of water, free hydrochloric acid, 
ferments, zymogens, and mineral acids; but an accurate analysis 
of the normal human gastric fluid is impossible, since this fluid 
is always contaminated with an admixture of sahva. It has been 
possible to obtain an analytic report of ai^alyses of the gastric 
juice in a case suffering from gastric fistula, and, according to 
Schmidt, the following table will designate the sohd constituents 
per thousand parts of gastric juice: 



ACIDITY. 321 

Water 994-4 

Solids 5.6 

Organic material 3.19 

Sodium chlorid i .46 

Calcium chlorid 0.06 

Potassium chlorid 0.55 

Ammonium chlorid not given. 

Hydrochloric acid 0.2 

Calcium phosphate | 

Magnesium phosphate >■ o.i 2 

Iron phosphates j 

It is to be borne in mind that in the foregoing analysis it was im- 
possible to exclude from the gastric juice the buccal secretions; 
hence the table, more correctly speaking, represents the chemic 
constituents of the gastric fluid when mixed with sahva. 



ACIDITY. 

Schmidt has satisfactorily shown that the acidity of normal 
gastric juice depends upon the presence of free hydrochloric acid. 
Experimentally it has been demonstrated that by determining 
the amount of chlorin and basic constituents present in the gastric 
juice the latter substances, after having been thoroughly saturated, 
still permit a quantity of hydrochloric acid to remain. In the 
dog this varies between 0.25 and 0.42 per cent. — average, 0.35 
per cent. It is generally conceded that the acidity of pure gastric 
juice is dependent upon the presence of free hydrochloric acid, 
but when contaminated with sahva or mixed with foods in the 
various stages of digestion, other factors are to be taken into 
consideration. 

After the ingestion of food, a varying amount of lactic acid, 
derived from the carbohydrates and acid salts, is also present; 
in fact, Ewald regards the gastric acidity during the early stage 
of digestion as depending, in a variable measure, upon the presence 
of lactic acid. It is to be borne in mind, however, that hydro- 
chloric acid is also present at this stage of digestion, but it prob- 
ably exists in rather close combination with albuminous sub- 
stances. Whenever the albuminous substances present in the 
stomach have become saturated, hydrochloric acid appears in 
the gastric contents, and this appearance is followed by a les- 
sening in the formation of lactic acid; the quantity of the latter 
gradually decreases, since hydrochloric acid inhibits the develop- 
ment of the micro-organisms concerned in the production of lactic 
acid. The degree of acidity to be noted at the different stages 
of digestion is illustrated by the accompanying charts, which 
have been designed by Rosenheim (Figs. 135, 136). In 



322 GASTRIC CONTENTS. 

disease the quantity of free hydrochloric acid may display wide 
variations, and in extreme conditions it may be absent (gastric 
carcinoma), or even reach a maximum point of 0.5 per cent, 
(gastric ulcer). Again, the quantity of lactic acid which, under 
normal conditions, is but slight or absent during the height 
of digestion, is often found increased, and fatty acids are hkely 
to be present at this time. 

The total acidity of the gastric contents will, therefore, be 
seen to depend upon the presence of some one or more of these 
acids, but a high degree of acidity does not point directly to the 
presence of any one acid in excess, and it is, therefore, necessary 
to determine the presence or absence of the various acids and of 
acid salts in order to determine upon what particular substance 
present the acidity depends. 

Tests for Free Acids. — i. Test the gastric contents with 
litmus-paper. 

2. The next step is to determine whether the acidity present 
be due to free acids or to acid phosphates: (a) Dip about one inch 
of a slip of Congo-red test-paper into the gastric fluid, when, in 
the presence of free acids, this paper is turned blue — a change 
not induced by acid phosphates; but should combined hydrochloric 
acid also be present in a large amount, this, too, will cause a blue 
reaction. 

Congo-red Test-paper. — Place one decigram of Congo red 
in 100 c.c. of water; cut bibulous paper in narrow strips, and 
soak them in this solution, from which they are to be removed and 
allowed to dry in the air. Place in a colored, glass-stoppered 
bottle. 

Congo-red test-paper is less dehcate than when the same 
reagent is employed in solution, and will only indicate the presence 
of o.oi per cent, of hydrochloric acid; but by using a weak solu- 
tion of Congo red, 0.0009 per cent, of hydrochloric acid may be 
detected. This is accomphshed by adding one or more drops of 
the Congo-red solution to from 5 to 10 c.c. of the filtered gastric 
juice. In the presence of free acids a blue color develops which 
will be seen to vary through the successive shades from that of a 
sky-blue to a deep azure. 

Place 5 c.c. of the gastric fluid in a test-tube and add to it a 
small amount of calcium carbonate. Should effervescence occur, 
free acid is present. Filter this fluid, and should the filtrate still 
retain its acidity, acid phosphates are present; free acids being 
neutrahzed by calcium carbonate, while acid phosphates are not 
materially influenced. 

Clinical Significance. — A negative result is conclusive evi- 



ACIDITY. 323 

dence that peptic activity is absent, since pepsin is active only in 
solutions that contain free acids. A positive reaction calls for 
further tests to determine the presence of free hydrochloric acid, 
lactic acid, or fatty acids. 

Total Acidity. — Reagents. — (i) A -^^ normal solution of 
sodium hydrate (4 gm. in 1000 c.c. of distilled water); (2) an 
alcohoHc solution of phenolphthalein (i per cent.). 

The total acidity of the gastric contents depends upon the 
following factors: Free hydrochloric acid; hydrochloric acid 
in combination; acid salts, and organic acids (lactic and butyric). 

Estimation. — The acidity of the gastric contents is ascer- 
tained by titrating a given quantity of gastric juice with the j^q 
normal solution of sodium hydrate, a few drops of the phenol- 
phthalein solution having first been added. 

Jaworski and Ewald have proposed calling the number of 
cubic centimeters of the sodium solution that are required to 
neutrahze 100 c.c. of the stomach-contents the "degree of acidity," 
and, indeed, this method, if universally employed, would in a 
measure simpHfy computation. 

Technic. — i. Place 10 c.c. of the gastric contents in a beaker. 

2. Add a few drops of the phenolphthalein solution. 

3. Add from a buret the y^ normal sodium-hydrate solution 
(a few drops at a time), stirring the mixture with a glass rod after 
each addition of the soda solution. 

4. At the point where the gastric contents assumes a dark 
flesh color its acidity has been neutrahzed by the sodium solution; 
and the number of cubic centimeters of the -^^ sodium-hydrate 
solution employed is read from the buret. 

Let us suppose that it required 4.8 c.c. of the -^-^ normal sodium- 
hydrate solution to neutrahze 10 c.c. of the stomach-contents: 
the decimal point is then removed one place to the right, giving 
us the figure 48, which figure represents the acidity of the stomach- 
contents. 

Normal. — Normal gastric juice will be found to give a figure 
between 40 and 60. 

The total acidity is also expressed in terms of HCl, and is 
readily calculated according to the well-known laws of molecular 
equivalents (1000 c.c. of the -^-^ normal solution contain 4 gm. 
of NaOH, which is equivalent to 3.65 gm. of HCl; should 50 
c.c. of the Y^Q- normal soda solution be needed to neutrahze 100 
c.c. of gastric juice, 2V of a Hter of the -^-^ normal soda solution 
was needed, or the equivalent to 2-V of ?>-^S g"^- of HCl). Hence 
the acidity of this 100 c.c. of gastric fluid is equivalent to that of 
0.18 gm. of HCl; in other words, the acidity is 0.18 per cent. 



324 GASTRIC CONTENTS. 

Under normal conditions the acidity in terms of HCl will be found 
to approximate 0.2 per cent. 

Hyperacidity. — A high figure is to be obtained in cases of 
gastric ulcer, gastric dilatation, gastric neurosis (less often), and 
where there is a hypersecretion of gastric juice. 

Under pathologic conditions the acidity of the gastric juice 
may not depend upon hydrochloric acid alone. In fact, the total 
acidity may be extremely high in gastric contents devoid of hydro- 
chloric acid, but rich in fatty and lactic acids. 

Hypoacidity. — The gastric juice may rarely be of an alkahne, 
neutral, or amphoteric (changes red Htmus-paper to blue and blue 
litmus to red) reaction, but it is rather unusual to obtain 
alkaline gastric fluid through the stomach-tube. The acidity 
of the gastric juice is lowered in the mucous forms of chronic 
gastritis, and where there has been a complete destruction of the 
gastric glands. I have found the reaction of the gastric fluid 
neutral upon several occasions, but without exception the patient 
either had taken a large quantity of fluid a short time before the 
recovery of the gastric contents or he was suft'ering from a chronic 
catarrhal condition of the throat, and consequently swallowing 
an excessive quantity of buccal secretion. 

When the gastric contents is collected by allowing the patient to 
eject it through the act of vomiting, an alkahne reaction is com- 
monly obtained, and this alkalinity is in part, if not entirely, due 
to the admixture of secretions from the throat and buccal cavities. 

Amount of Hydrochloric Acid. — In health, pure gastric 
juice has been estimated by Ewald, Boas, and Szabo to contain 
from 0.2 to 0.3 per cent, of free hydrochloric acid. Such quan- 
tities of hydrochloric acid are to be found only in gastric juice 
obtained at the height of digestion, after all the albuminous and 
basic affinities have been satisfied. The exact period at which 
this height of digestion is reached is governed by the character 
.and the quantity of the food and hquids previously ingested: 
the less work there is to be accomphshed, the sooner will the 
gastric contents be found to contain free hydrochloric acid fol- 
lowing the ingestion of food. Following the ingestion of Ewald's 
test-breakfast the hydrochloric acid appears in from thirty to 
thirty-five minutes; but the point of maximum intensity is usually 
reached in from fifty minutes to an hour, and may correspond 
to 1.7 to 0.17 per cent. (Fig. 135). Mler the administration of 
Riegel's meal the free acid appears after one hundred and thirty-five 
minutes, and reaches its highest point, corresponding to 0.27 per 
cent., in from one hundred and eighty to two hundred and ten 
minutes (Fig. 136). 



ACIDITY. 



325. 



P.M. 

3.0 ' 



2-5 



1-5 



075 



0-5 



0.25 



li 



I 



10 20 



40 50 60 70 80 90 100 



Fig. 135.— Illustrating the curve of acidity after Ewald's test-breakfast: ^, Hydrochloric 
acid ; ---, lactic acid ; X, beginning of the stage of free hydrochloric acid (Rosenheim). 



L^ L_^^ ^ \ 1_ ^^, ^j — I 




^iiSbi^^^^^^=^i^^iii^i^^^i^^^^ 


1" ' ■ ~ " 




i 






1 1 1 iJt^mi mi^ li 1 


MMtiiM 


1 J^i 1 1 1 1 1 mm 1 

7 - ~ 


-"'i -?:::: - -- : -:: — : — ""^^ " - - 


:::z^::^:::::::::::::i:::::::::i:i5i^-::::::::::: 


Mil n I' 1 


:^^^::::::::::::::::::::::::::=:ii::i::::::::::::: 


^:::::: :: ::::::::::::::: ::::::i:ii:::::::::::::::i 



Fig. 136.— Illustrating the curve of acidity after Riegel's test-meal: a^, Hvdrochloric acid 
---, lactic acid ; X, beginning of the stage of free hydrochloric acid (Rosenheim). 



326 GASTRIC CONTENTS. 

The following terms are applied to designate the degree or 
proportion of hydrochloric acid secreted: EucJilorkydria, a secre- 
tion of the normal amount of free hydrochloric acid, varying 
from 0.1 to 0.2 per cent.; JiypercJiIorhydria, the secretion of more 
than 0.2 per cent.; hypocJilorhydria, the secretion of less than o.i 
per cent.; and anchlorJiydria, where no hydrochloric acid at 
all is secreted. 

Euchlorhydria. — This condition is most frequently observed 
in connection with nervous dyspepsia, and is always to be found 
where no gastric derangement exists. 

Rarely a normal secretion of free hydrochloric acid is found 
where atony of the muscular wall of the stomach exists. The 
presence of a normal amount of free hydrochloric acid tends to 
exclude the existence of chronic gastritis and favors the presence 
of the so-called nervous dyspepsia. 

Hyperchlorhydria. — A hypersecretion of hydrochloric acid, as 
a rule, indicates gastric neurosis, and is commonly encountered 
in the gastric fluid of neurasthenic persons. A hypersecretion 
of hydrochloric acid is at times coupled with a continuous hyper- 
secretion of gastric juice. 

H}perchlorhydria is commonly encountered in cases of gas- 
tric ulcer, and in three instances I have observed it in gastric 
carcinoma. Theoretically, and probably in every instance of 
this nature, the gastric carcinoma was preceded by, and may be 
developed at the site of, an old ulcer. 

Hypochlorhydria. — This condition is associated with patho- 
logic states where the secretory power of the stomach is inhibited 
or lessened as a result of disease; and is to be observed in con- 
nection with subacute and chronic gastritis, duodenal ulcer, gas- 
tric carcinoma, dilatation, atony, and, rarely, in cases of gastric 
ulcer. 

Anchlorhydria. — This condition is most commonly met in 
gastric carcinoma, although an absence of free hydrochloric 
acid is not essentially to be found in this disease, as has been 
set forth under hyperchlorhydria. Anchlorhydria may be 
observed in connection with chronic gastritis and in neurasthenic 
individuals. It Avill be found that the degree of acidity of the 
gastric contents will fluctuate within wide limits during the course 
of the various chronic diseases, and especially in those placarded 
by cachexia and emaciation. 

Source and Significance of Hydrochloric Acid. — It is not 
the purpose of this volume to deal with the physiology of the 
gastric secretion and of its one important constituent, hydrochloric 
acid. It will suffice, however, to state that the hydrochloric acid 



ACIDITY. 327 

is not derived from the chlorids ingested; its secretion is continu- 
ous, and the total acidity of the stomach-contents in no way 
depends entirely upon the quantity and the quality of the food 
taken. The chlorids of the blood furnish the necessary chlorin 
to the gastric contents. A fact ever to be borne in mind is that 
the pyloric glands furnish an alkaline secretion, while the glands 
of the fundus furnish an acid secretion. It is thought that the 
parietal cells are concerned in the production of hydrochloric 
acid. A further and more elaborate description of the physi- 
ology of this secretion has been omitted because the entire sub- 
ject of the production of hydrochloric acid remains undetermined. 
(The reader is referred to special works upon physiology and phys- 
iologic chemistry for a more complete discourse upon this subject.) 

It seems clear that the factor to be concerned in the production 
of hydrochloric acid is a normal condition of the blood and of the 
secretory cells. Experience shows that whenever any decided 
abnormality exists in either the blood or the secretory cells, hydro- 
chloric acid is secreted in abnormal quantities; or, in fact, there 
may be no secretion whatever. A consideration of serious im- 
portance is the condition of the general nervous system, since 
nerve energy figures largely in many forms of gastric derange- 
ment and since the cells are dependent upon this tissue for their 
innervation. Circulatory embarrassment of the stomach may 
result in impaired nutrition of the secretory cells, whether this 
condition be inflammatory or otherwise, and it is for this reason 
that the gastric secretion is materially altered during the course 
of inflammatory processes of the stomach, tumors, congestion, 
and during such chronic conditions as nephritis, hepatic cirrhosis, 
pulmonary tuberculosis, valvular heart disease, and, in fact, aU 
conditions accompanied by anemia. Here may be the opportune 
place to make mention of the fact than an analysis of the gastric 
contents is of but limited value where the patient is suffering from 
anemia, either primary or secondary, the cause of which is not of 
gastric origin. 

Function. — The reader is referred to special works on phy- 
siology for the functions of the hydrochloric acid. From a chnical 
as well as from a physiologic standpoint the antiseptic proper- 
ties of the hydrochloric acid become of special importance. 

It has been shown by various observers that hydrocliloric 
acid possesses a germicidal power under certain conditions; 
and it has been further proved that normal gastric juice destroys 
the cholera bacillus, Streptococcus pyogenes, Staphylococcus 
pyogenes aureus, bacillus of anthrax, Shiga's bacillus, and numer- 
ous other pathogenic bacteria. It is worthy of mention that 



328 GASTRIC COXTEXTS. 

the tubercle bacillus is not destroyed by gastric juice, and that 
a portion of the spores of anthrax escape destruction when placed 
in the gastric fluid. Hydrochloric acid inhibits the development 
of the bacteria concerned in the production of lactic and butyric 
acids, although these eventually escape complete destruction, 
since they are always present in the gastric fluid when the degree 
of hydrochloric acid is at a Ioav ebb, as has been described under 
Acidity (page 32 ij. 

Tests for Free Hydrochloric Acid.^It may prove of value 
to the student to know a number of reagents in the order of their 
delicacy, through the use of which it is possible to detect free hydro- 
chloric acid in the filtered gastric juice: 

Dimethylamido-azobenzcl o.c2 pro mille. 

Phloroglucin-vanillin 0.05 '' " 

Resorcin 0.05 " " 

Congo red 

Tropgeolin 00 0.3 " " 

Emerald-green 0.4 " " 

Mohr's reagent i.o " " 

Dimethylamido-azobenzcl. — This test is extremely dehcate, 
and its accuracy has been such that it is personally recom- 
mended most heartily to the profession. To demonstrate its 
dehcacy the reagent is employed where a neutral yellow indi- 
cator has been added, and is changed to a reddish or cherry tint 
upon the addition of but one drop of a -^-^ normal solution of 
hydrochloric acid in 5 per cent, of distilled water. A red color is 
also produced with organic acids, should they be present in amounts 
above 0.5 per cent., but this reaction is prevented whenever small 
quantities of mucin, peptones, or albumin are present; and since 
one or more of these bodies are commonly present, it is seldom, 
if ever, that the reaction is caused by organic acids unless a much 
larger amount is present. Xo color is produced by the loosely 
combined hydrochloric acid nor by the acid salts. 

Method. — Reagents. — A 0.5 per cent, alcoholic solution of 
dimethylamido-azobenzol : (i) Place 5 to 20 c.c. of filtered 
gastric contents in a test-tube (it is not essential that the 
contents be filtered, though it is my practice to filter^; (2) hold 
this test-tube in a good light, and add to it, from a pipet, one to 
three drops of dimethylamido-azobenzol solution. 

If free hydrochloric acid is present, a cherry-red color is 
formed (Plate 2 2\ the intensity of which varies in direct ratio 
to the quantity of free acid present. Should there be no free 
hydrochloric acid present, the fluid becomes cloudy, at times 
fluorescent, or may assume a yellowish tint. The reaction changes 



PLATE 22. 




« c;:: ^ -^ w "z; 



k. 



U. ^-1 ^J 



u: w in ta a ^ 
03 c3 ra ^ _^ , , 



<P3U< WU 



ACIDITY. 329 

to a yellow when titrated with a decinormal solution of sodium 
hydrate (hydroxid), as shown by Plate 22, C and C^ 

Phloroglucin-Vanillin Test. — Reagents. — Place in a mortar 
2 gm. of phloroglucin and i gm. of vanilhn and dissolve in 
30 c.c. of absolute alcohol. This solution is at first of a yellow 
color, which gradually darkens to a golden-red, and if exposed 
to the light, changes to a brown. Keep in a colored glass-stop- 
pered bottle. 

It has been recommended that the two substances be kept 
in separate solutions, and that two or more drops of each be mixed 
when the reagent is to be used. 

According to Boas, the above solution will be found shghtly 
more delicate and decidedly more staple when the above propor- 
tions of the phloroglucin and vanilHn are dissolved in 100 gm. of 
80 per cent, alcohol. 

Method. — Place a few drops, or, if desired, a few cubic centi- 
meters, of filtered gastric contents in a dish or in a test-tube, 
and to it add an equal quantity of the reagent. No change 
occurs until the mixture is gently heated, — avoid boiling and 
evaporation! — when in the presence of 0.05 per cent, or more 
of free hydrochloric acid fine rose-colored lines form throughout 
the mixture. I prefer to carry on the reaction in a porcelain dish 
or cover (Plate 23), allowing the evaporation to take place slowly, 
when a rose color is indicative of the presence of free hydrochloric 
acid. The intensity of this color varies in direct proportion to 
the quantity of free hydrochloric acid present. Should the dish 
be heated at too high a temperature, a brown, brownish-yellow, 
reddish, or reddish-brown color is obtained; a similar result is 
at times obtained in the absence of free hydrochloric acid. 

This reaction is not induced by the presence of organic acids, 
nor do they in any Avay interfere with the reaction; neither is it 
affected by albumins, peptones, or acid salts. 

Test-paper. — Certain workers prefer to prepare a test-paper by 
soaking narrow strips of ash-free filter-paper in the test solution, 
and further to prepare and employ this paper as directed under the 
dimethylamido-azobenzol test (page 328). After the filter-paper 
is moistened with a drop of gastric fluid it is to be placed in a 
porcelain dish and heated gently. In the presence of free hydro- 
chloric acid a rose color develops which is not altered by ether. 

Resorcin Test. — Reagent. — Dissolve 5 gm. (7.7 gr.) of resub- 
hmed resorcin and 3 gm. (4.4 gr.) of cane-sugar in 100 gm. 
(3.5 oz.) of 94 per cent, alcohol. Keep in a colored glass-stoppered 
botde. 

Reaction. — i. Place from three to five drops of the fihered 



330 GASTRIC CONTENTS. 

gastric juice in a porcelain dish, and to it add an equal quantity 
of the reagent. 

2. Grasp the dish firmly in a pair of forceps, and hold it 
sufficiently close to the flame of a Bunsen burner to cause a slow 
evaporation of the liquid, continuing the heat evaporating to 
dryness; when in the presence of free hydrochloric acid a rose 
or vermilion-red mirror occupies the surface of the porcelain which 
was at first covered by the Kquid (Plate 23). 

Immediately surrounding the mirror is a zone of variable 
brown shade. The intensity of this color fades upon cooling. 

It is also possible to prepare test-paper from this reagent, 
and to test the gastric contents according to the technic described 
in connection with the dimethylamido-azobenzol test. This 
test-paper, when dipped into the gastric contents, is turned a 
violet color, and later, upon the application of heat, changes to a 
brick-red, which does not change when treated with ether. The 
resorcin test is in no way influenced by the presence of organic 
acids, albumins, peptones, or by acid salts. It has been used 
daily in my laboratory during the past five years. 

Congo-red Test. — Reagent. — An aqueous solution of Congo 
red, i-iooo. 

Method. — I. Fill the test-tube to one-half its depth with water 
and to it add three drops of the reagent (Plate 23, B). 

2. Grasp this tube between the thumb and index-finger, 
hold it in a clear light, and allow one or two drops of the gastric 
contents to fall from a pipet. Hold the tube steady to prevent all 
jarring. Immediately upon the drop of gastric contents coming 
in contact with the red solution a blue color is produced, the upper 
portion of the liquid changing to a pale and then to a dark blue, 
and, as the gastric contents traverses through the lower, red 
stratum of the liquid, it leaves behind a faint blue track, collecting 
at the bottom of the tube in the form of a light-blue sediment 
(Plate 23, B^). When the reaction is allowed to stand for a time, 
it may at first deepen, but later it is noticed to fade. 

Congo red was first recommended as a test for free hydrochloric 
acid by von Hosslin and by Riegel in 1886, these authors sug- 
gesting that it be used in the form of test-paper. Through personal 
experience I have been unable to obtain satisfactory results in 
this manner. I have employed the Congo-red test in solution, 
as above outHned, during the past six years, and thus far have 
had no reason to change to any other test for general routine 
work. 

Fallacies. — True, indeed, the Congo-red test is subject to 
certain fallacies, as are most reactions for free hydrochloric acid, 



ACIDITY. 331 

and it is not to be used to the exclusion of all other tests. Per- 
sonally, I employ the Congo-red and the resorcin test in every 
instance. 

Organic Acids. — It is worthy of note that free organic acids 
are capable of changing Congo red to blue, but these acids are 
seldom, if ever, present in the gastric contents in sufficient amounts 
to induce this change. No color change occurs with combined 
hydrochloric acid, and the reaction is not influenced by albumins 
or by acid phosphates in such dilution as they are met with in 
the stomach-contents. 

Tropgeolin Test. — Reagent. — A saturated alcohohc solution of 
tropseohn 00. This reagent is of a brown-yellow color. 

1. Place four or five drops of the reagent in a porcelain dish; 
grasp the dish with a forceps, and tilt it from side to side so that 
the reagent may flow over a large area of its surface. 

2. An equal quantity of the gastric contents is now added, and 
in a like manner encouraged to flow over the surface of the dish. 

3. Heat the dish gently over a Bunsen flame, avoiding ex- 
cessive temperature; in the presence of free hydrochloric acid 
a lilac shade or faint blue Hues appear. Boas has found this 
reagent to indicate the presence of free hydrochloric acid where 
this substance exists in from 0.2 to 0.3 per cent. For practical 
work this test will be found satisfactory, but in instances where 
a negative result is obtained, the more dehcate reactions previously 
described are to be employed. 

A test-paper may be prepared from this reagent, and when 
saturated with the gastric contents and gently heated, changes 
to the characteristic lilac or blue. In the presence of organic 
acids a brown color develops, but this disappears upon the 
application of heat; and at no time during the reaction is a lilac 
or blue color caused by organic acids. 

Mohr^s Test. — Reagent. — Place 2 c.c. of a 10 per cent, 
solution of potassium sulphocyanid and 0.5 c.c. of a neutral solu- 
tion of ferric acetate in a graduate, and to the mixture add 10 c.c. 
of distilled water. This reagent is of a ruby-red color. 

Reaction. — Place two to five drops of the reagent on a porcelain 
dish, and to it add an equal quantity of the filtered gastric con- 
tents. Place the reagent and the stomach-contents on different 
sides of the dish and permit them gradually to come in contact. 

Free hydrochloric acid induces a Hght violet color which is 
deepest at the line of contact of the reagent and the gastric 
fluid. When the fluid and reagent have been well mixed, a deep 
mahogany color is seen. Mohr's test cannot be regarded as a 
liighly sensitive one, and while it is not influenced by the presence 



S3^ GASTRIC CONTEXTS. 

of acid salts or of peptones, it should not be employed to the 
exclusion of other tests. 

For a description of CipoUino's test see p. 533. 

Quantitative Estimation of Hydrochloric Acid. — Topfer's 

Method. — Topfer's method for the estimation of hydrochloric 
acid in the gastric contents will be found sufficiently accurate 
for practical laboratory studies, and has to recommend it the 
important feature that analysis by this method is easy of execu- 
tion. 

Reagents. — (i) A decinormal solution of sodium hydroxid 
(see page 323). (2) A solution of phenolphthalein (i per cent.). 
(3) An aqueous solution of ahzarin (i per cent.). (4) An alcohohc 
solution of dimethylamido-azobenzol (0.5 per cent.). 

The first step in this technic is to estimate the total acidity, 
according to the method previously described (page 323), em- 
ploying a given amount of gastric juice. This total acidity 
represents that due to free hydrochloric acid, combined hydro- 
chloric acid, organic acids, and the acid salts present. Where 
lactic acid and the fatty acids are found to be present in the given 
gastric contents, it is not essential that these be removed before 
estimating the hydrochloric acid. Alizarin or monosulphonate 
of soda is also employed as an indicator, since it reacts when in 
an alkahne medium. The third step in Topfer's test is to esti- 
mate the quantity of free hydrochloric acid, which is done by 
using dimethylamido-azobenzol as an indicator. 

Method. — Place from 5 to 10 c.c. of filtered gastric juice into 
each of three small beakers, or, preferably, into three test-tubes 
(Plate 22). 

1. To the first of these tubes add two drops of phenolphthalein 
(Plate 22, A), when the fluid will be seen to take a hght-grayish 
hue. Titrate the solution in tube A with a y^- normal solution 
of sodium hydrate until a pink color appears, at which point the 
Y^Q- normal solution should be added, a few drops at a time, until 
a permanent red color is obtained (Plate 22, A^). The process 
of titration must be continued until the red color does not disap- 
pear when the tube is allowed to stand for a time and its contents 
does not become intensified upon the addition of a few drops of 
the sodium solution (end- reaction). Read from the buret the 
number of cubic centimeters of the y-jj normal sodium solution 
that were required to neutralize the known quantity of gastric 
contents. 

2. Add four drops of ahzarin solution to the second tube, 
when the contents of the tube will assume a yellowish hue (Plate 
22, B). Titrate this mixture with a y-^ normal solution of sodium 
hydrate until a decided violet color is obtained (Plate 22, B)'. 



PLATE 23. 





A. Uffelmann's reagent. 

A'. A after the addition of gastric fluid containing lactic acid. 

B. Water to which three drops of Congo -red solution have been added. 

B'. Change induced in B when gastric fluid containing free hydrochloric acid 
is added. 





1. Resorcin test for free hydrochloric acid. 

2. Giinzburg's test for hydrochloric acid. 



ACIDITY. 333 

With the aid of the accompanying illustrations (Plate 22, B, B') 
there will be little or no difficulty for the inexperienced to follow 
closely this technic. 

3. To the gastric contents in the third tube add three or four 
drops of dimethylamido-azobenzol, when a red or rose hue is 
produced (Plate 22, C). Should there be no free hydrochloric 
acid present in the gastric contents, a yellow instead of a red 
color follows the addition of the dimethylamido-azobenzol solu- 
tion. Titrate this red mixture with a yV normal solution of sodium 
hydrate until all the red color has disappeared and the hquid 
changes to yellow (Plate 22, C). 

Computation. — Let us suppose that 10 c.c. of gastric contents 
are placed in each of the three test-tubes. In the first 10 c.c, 
phenolphthalein being used as an indicator, it required 10 c.c. 
of the tV normal solution to effect the terminal or end-reaction 
(permanent red); but an equal quantity of gastric contents to 
which ahzarin had been added as an indicator required only 7 
c.c. to induce the end-reaction. It will be readily seen that the 
difference between the quantity of the tV normal solution employed 
to neutralize the 10 c.c. of gastric contents containing phenol- 
phthalein and that needed to neutralize the 10 c.c. containing 
alizarin equals 3 c.c. This quantity of the yV normal solution 
(3 c.c.) indicates the amount required to neutrahze the hydrochloric 
acid which was in combination with albuminous substances. 

One cubic centimeter of the yV normal solution corresponds 
to 0.00365 gm. of hydrochloric acid; hence the amount of hydro- 
chloric acid combined with albuminous substances present in 
the 10 c.c. of gastric contents examined is estimated by multiply- 
ing 0.00365 by 3, which gives 0.01095 gm. of hydrochloric acid; 
and this figure is also employed as 0.01095 P^^ cent. 

Combined Hydrochloric Acid. — The total acidity of the 
gastric contents depends in a measure upon the presence of loosely 
combined hydrochloric acid, and since this hydrochloric acid 
is essential to digestion, it is of great importance to ascertain 
whether or not combined hydrochloric acid be present in a given 
gastric contents, even where free hydrochloric acid be absent. 
The presence of free hydrochloric acid in normal quantities im- 
plies that peptic digestion is taking place, and, further, indicates 
that all the albuminous affinities present in the gastric contents 
have been satisfied, free hydrochloric acid appearing as such after 
all albuminous substances have been saturated. Free hydro- 
chloric acid may be absent and still there may have been a certain 
quantity of hydrochloric acid secreted, and this acid be in com- 
bination with albuminous substances, the amount secreted being 



334 GASTRIC CONTENTS. 

only sufficient to satisfy a portion, or possibly all, of the albuminous 
affinities, in which case peptic digestion, which is active only in 
the presence of free hydrochloric acid, does not progress. 

It is readily seen, therefore, that a knowledge of the combined 
hydrochloric acid is of great importance in connection with most 
gastric disorders, particularly those wherein free hydrochloric acid 
is absent from the gastric contents. 

An entirely different condition exists where both free and 
combined hydrochloric acid is absent from the gastric contents, 
and implies that no hydrochloric acid is secreted. Where this 
condition exists, the stomach acts merely as a storehouse for pro- 
teids. 

Free Hydrochloric Acid. — The estimation of the free hydro- 
chloric acid is made for lo c.c. of the gastric contents, using 
dimethylamido-azobenzol as an indicator. Let us suppose that 
3.5 c.c. of the To" normal solution were required to produce the 
end reaction, then 0.00365 X 3.5 = o. 01 1675, or o. 01 1675 percent. 

It will be remembered that in ascertaining the total acidity 
of 10 c.c. of gastric contents 10 c.c. of a yV normal sodium-hydrate 
solution were required, which, in terms of hydrochloric acid, are 
equivalent to 10 X 0.00365 = 0.0365 gm. of hydrochloric acid, or 
0.0365 per cent. Deduct from this number the sum of the amount 
of both free and combined hydrochloric acid, 0.01095 + ^•^'^^SIS 
= 0.023725; 0.0365 — 0.023725, or 0.012775 per cent., which 
equals the percentage of acidity due to organic (lactic and butyric) 
acids. 

Clinical Significance. — In selecting a diet for an individual 
where the hydrochloric acid is known to be absent it is neces- 
sary to direct that proteids be given in such form as will permit 
them to be subject to pancreatic digestion, obviating all possible 
delay. It is in such conditions that the administration of pre- 
digested foods is indicated. 

At times it is found that the quantity of hydrochloric acid 
secreted is sufficient to satisfy the albuminous affinities of a mod- 
erate-sized meal in which the proteids have been limited, and in 
such cases, when a suitable dietary be followed, digestion may 
go on perfectly. It is also possible to give a favorable prognosis 
where this amount of hydrochloric acid is secreted; but where 
there is an absence of loosely combined hydrochloric acid, this 
finding points to a destruction of the glandular elements of the 
stomach, in which instance prognosis must, of necessity, be grave. 

Tests for combined hydrochloric acid have been described 
in connection v^th Topfer's test for free hydrochloric acid (page 
332). 



FERMENTS AND THEIR ZYMOGENS. 335 

FERMENTS AND THEIR ZYMOGENS. 

It is generally conceded that pepsin itself is not secreted as a 
product of the chief cells of the glands of the fundus, but that 
the zymogen of pepsin (pepsinogen or propepsin) is secreted. 
Numerous experiments have proved this statement, and shown 
that in fasting animals the glands of the stomach do not contain 
pepsin, but a substance which is not destroyed by sodium car- 
bonate and which is readily converted into pepsin when brought 
in contact with hydrochloric acid. It is this substance which 
has been designated under the caption pepsinogen. 

Pepsin is to be recovered from the mucous membrane of the 
stomach during the stage of digestion, but during the non-digestive 
stage, zymogen is to be recovered. Zymogen may be found 
coexistent with pepsin in the normal gastric juice recovered 
during the process of digestion. The time at which zymogen is 
transformed into a ferment is doubtful. A fair amount of evidence 
exists, however, to show that this change takes place after it has 
been secreted. 

Destruction. — Pepsin and the activity of its ferment are 
destroyed by dilute solutions of alkaline carbonates or exposure 
of a solution of pepsin to 70° C. (158° F.); but pepsin in the dry 
state is not destroyed by a temperature of 100° C. (212° F.). 

It is to be borne in mind that albuminous substances may be 
digested by pepsin wdien in the presence of hydrochloric acid and 
certain other acids, as sulphuric, acetic, phosphoric, salicylic, and 
lactic. A solution of any one of these acids must needs be con- 
siderably stronger than is needed when the acidity is due to 
hydrochloric acid. Hydrochloric acid requires from two to four 
pro mille to obtain satisfactory results, but should we employ 
lactic, 12 to 18 pro mille would be necessary to accomplish the 
same end. In this connection the experiments of Petit are of 
speciaP importance, since this observer found that a preparation 
of pepsin would digest 500,000 times its weight of fibrin in a 
period of about seven hours. It is again important that extremely 
small quantities of pepsin are always capable of digesting large 
quantities of albuminous substances. 

The quantity of pepsin or of its zymogen secreted during the 
twenty-four hours can only be approximated from the apparent 
peptic activity, which is estimated through the amount of albu- 
minous substances digested; and it is to be remembered that this 
will be found to fluctuate within wide Hmits under normal con- 
ditions, depending in a great measure upon the degree of con- 
centration of the free acid present. 



2,z(i GASTRIC CONTENTS. 

Clinical Significance. — While the study of free hydrochloric 
acid and that of pepsin have been considered side by side in this 
volume, it is to be emphasized that the recognition of pepsin in 
relative amounts concerns us more than does that of free hydro- 
chloric acid. It has been stated that pepsin is formed from pep- 
sinogen when in the presence of free acid. Therefore the absence 
of organic acids in appreciable quantities is conclusive evidence 
that free hydrochloric acid is present and that peptic digestion 
is active. On the other hand, when free hydrochloric acid is 
found, pepsin, as a rule, is present, though the reverse condition 
may exist. When hydrochloric acid is added to the gastric con- 
tents and the fluid is then found incapable of digesting albumins, 
both pepsin and its zymogen are absent ; but should the zymogen 
be present, digestion occurs after the addition of an acid. In 
rare instances the gastric juice is found to be capable of digesting 
albumins without the admixture of hydrochloric acid, such diges- 
tion depending upon the presence of pancreatic secretion. 

Impaired gastric circulation and nervous conditions of the 
stomach affect but slightly, if at all, the production of pepsin; 
and a diminution or an absence of pepsin or its zymogen is refer- 
able to a pathologic condition of the gastric glands. These 
features are most valuable in distinguishing- between gastric 
neurosis, chronic gastritis, and hyperemia of the gastric mucosa, 
the result of circulatory embarrassment. 

Test for Pepsin and Pepsinogen. — Test a portion of the 
filtered gastric contents for the presence of free hydrochloric 
acid. Should this be present, proceed as follows for the detec- 
tion of pepsin and zymogen: 

1. Place 25 c.c. of the filtered gastric contents in a beaker, 
and to it add 0.05 to 0.06 gm. of egg-albumen. 

2. Place in an incubator, at a temperature of 37° to 40° C. 
(98.6° to 104° F.), for a period of three hours. 

Under normal conditions this quantity of gastric juice thus 
environed will have digested the egg- albumen. Fibrin and serum- 
albumin may be added instead of the egg-albumen, the former 
being digested in one and one-half hours, the latter, in one 
hour. 

Zymogen. — Should the gastric contents not contain free 
hydrochloric acid, giving negative results with the resorcin and 
Congo-red tests, proceed in the following manner: 

1. Place 25 c.c. of filtered gastric contents in a beaker, and to 
it add from three to five drops of an official solution of hydrochloric 
acid. 

2. Add the same quantity of egg-albumen, fibrin, or serum- 



FERMENTS AND THEIR ZYMOGENS. 337 

albumin that was added when hydrochloric acid was present 
(0.05 to 0.06 gm.). 

3. Place in an incubator at a temperature of 37° to 40° C. 
(98.6° to 104° F.), as described under the test for pepsin. Zymo- 
gen (pepsinogen) will, as a rule, be found. 

Quantitative Estimation of Pepsin. — Thus far I am not 
aware of any accurate method by which the amount of pepsin 
may be estimated, and the method of Hammerschlag, herein 
outHned, is capable of ascertaining merely relative values. 

Place three Esbach tubes in a tube-rack, and back of these 
tubes insert a piece of white cardboard upon which the figure 
corresponding to each tube is marked, i, 2, 3. Rosenburger's 
tube-rack will serve well for this purpose. 

Tube I. — Place in this tube a mixture of a one per cent, solu- 
tion of serum-albumin in 4 per cent, of hydrochloric acid, filHng 
to the mark U; then add 5 c.c. of filtered gastric juice, and place 
in the rack. 

Tiihe 2. — Fill this tube with the serum solution to the mark U, 
and add to it 0.5 gm. of pepsin. 

Tiihe 3. — Fill with the serum solution to the mark U, and add 
5 c.c. (i fi. oz.) of water. 

Place the rack and its contained tubes at a temperature of 
37° C. (98.6° F.) for one hour, then remove, and to each tube 
add Esbach's reagent (see page 211), filling to the mark R. 

After the addition of the reagent place the rubber stopper in 
position, grasp the extremities of the tube between the thumb and 
index-finger of each hand, and invert the tube slowly several times 
in order to effect a perfect minghng of the reagent through the 
mixture. Replace the tubes in the rack in their respective pockets, 
and allow it to stand at a temperature of 18° to 20° C. (64.4° to 
68° F.) for twenty-four hours. The amount of precipitated 
albumin is read from each tube, and that of tube i and 3 are com- 
pared by the reading given by tube 2, to which 0.5 gm. of pepsin 
was added, and which serves as the standard. 

Absence of Pepsin. — Jaworski has suggested a method 
wherein it is possible to ascertain whether the gastric contents 
be absolutely free from pepsin, the enzyme, and its zymogen: 
Introduce into the empty stomach, through a tube, 200 c.c. of a 
decinormal solution of hydrochloric acid, and permit this solution 
to remain for one hour. Again insert the tube, and extract the 
stomach-contents. Should this fluid be found to be free from 
pepsin, it is indicative that both the enzyme and its zymogen are 
absent. 

Test for Pepsinogen.— Boas has detailed a method of deter- 



338 GASTRIC CONTENTS. 

mining the relative proportion of pepsinogen present in the gastric 
contents. 

1. Place in a number of test-tubes a mixture of gastric con- 
tents and distilled water, diluting the gastric fluid at different 
strengths in these tubes — e. g., place in tube i a dilution of 1-5; 
tube 2, i-io; tube 3, 1-20; tube 4, 1-30, etc. 

2. Place these tubes in a rack, and number as described under 
the estimation of pepsin (page 337). 

3. Add to each tube a definite amount of egg-albumen. 

4. Place in an incubator at a temperature of 37° to 40° C. 
(98.6° to 104° F.). 

Note carefully which of the fluids is of sufficient strength to 
digest the albumin — the one of greatest dilution capable of accom- 
phshing this end represents the amount of pepsinogen present; 
the greater the degree of dilution, the more plentiful the pepsin- 
ogen. 

Chymosin. — The profession is indebted to Hammarsten for 
the original information concerning the milk-curdhng ferment and 
its zymogen (chymosin and chymosinogen). At present, Boas 
probably deserves credit for having brought forth most of the 
valuable information concerning this ferment and its proenzyme. 
The principal function of these substances appears to be exercised 
upon milk, or upon solutions containing a variable amount of 
casein, when rendered alkahne by preparations of hme. Casein 
is coagulated when in a feebly acid, alkaline, or neutral solution. 

The proenzyme is supposed to be formed by the cells of the 
gastric mucous tissue, though a neutral aqueous extract of the 
gastric mucous membrane is not likely to contain this ferment, 
but will usually contain its zymogen. The addition of free hydro- 
chloric acid is followed by the appearance of the ferment. 

An active solution of chymosin w^hen in the presence of free 
hydrochloric acid (3 pro mille) is found to be active when kept 
at a temperature of from 37° to 40° C. (98.6° to 104° F.); but 
pepsin, when thus environed, does not induce destruction. Again, 
zymogen is converted into an active ferment when the solution 
containing it is alkahnized by a solution of calcium chlorid, thus 
showing that in the presence of such salt free hydrochloric acid 
is not essential to this transformation. 

Both chymosin and its zymogen are physiologically present 
in the gastric secretions, thus rendering an accurate knowledge 
of the proportionate amounts of these bodies present of clinical 
value. The detection of chymosin in the vomit serves as cne 
of the valuable tests whereupon alkahne vomit is determined to 
be of gastric origin. 



FERMENTS AND THEIR ZYMOGENS. 339 

Qualitative Tests for Chymosin. — i. Place 5 to 10 c.c. of 
milk in a test-tube or into a beaker, and treat with from three 
to five drops of filtered gastric juice. 

2. Place in an incubator at a temperature of from 37° to 40° 
C. (98.6° to 104° F.) for fifteen minutes. 

In the event of coagulation having taken place at the end of 
this period, the enzyme is present. 

Tests for Chymosinogen. — i. Place 10 c.c. of filtered gastric 
juice in a test-tube. 

2. Render the gastric contents feebly alkaHne by adding two 
or more cubic centimeters of a solution of calcium chlorid (i per 
cent.). 

3. Place the mixture at a temperature of 37° to 40° C, when, 
should zymogen be present, a thick, caseous coagulum forms 
within a few minutes. 

Quantitative Estimation of Chymosin. — I am not aware 
of any method by which it is possible to determine, with any 
degree of accuracy, the quantity of enzyme present in a given 
gastric contents; and it is only possible, through the method here 
given, to ascertain merely relative values. Normal gastric juice 
will be found to give a reaction for the enzyme when diluted in 
the proportion of 1-30 or even 1-40. 

1. Place in each of three to six test-tubes a definite quantity 
of gastric juice. 

2. Place these tubes in a rack, and label A, B, C, D, E, F. 
Water is now added to each of the tubes, in such proportions as 
will effect in tube A a dilution of 1-5; B, i-io; C, 1-15; and so 
on, until we reach a dilution of 1-30, the minimum dilution at 
which the enzyme should be active. 

3. Add to each of the tubes a definite quantity of neutral 
milk. 

4. Place the tubes at a temperature of from 37° to 40° C» 
(98.6° to 104° F.), and observe carefully the point of greatest 
dilution at which coagulation takes place. 

At times the milk added may be found of an amphoteric 
reaction — turns red litmus-paper blue and blue litmus-paper 
red. Should coagulation occur at a dilution of 1-30, the enzyme 
is present in the minimum normal amount. 

Quantitative Estimation of Chymosinogen. — i. In estimat- 
ing the quantity of the zymogen present, tubes are arranged and 
labeled as described for the estimation of enzyme. 

2. Place in each of the tubes an equal quantity of milk. 

3. Add the feebly alkafine gastric juice to the various tubes in 
different quantities, producing a different dilution in each tube. 



340 GASTRIC CONTENTS. 

This process is further conducted in the manner described 
for the estimation of the enzyme, allowance being made for the 
quantity of the alkahne solution needed to alkahnize the gastric 
juice. Under normal conditions a dilution of from i-ioo or even 
1-150 will be found to give positive results. 

Clinical Significance. — Zymogen, when noted to be present 
in the gastric contents at several examinations after the admin- 
istration of Ewald's test-meal, is valuable evidence and serves 
to exclude the existence of organic disease of the stomach, 
pointing rather directly, as it does, to gastric hyperemia, neurosis, 
etc., conditions referable to disease outside the stomach. Where 
the zymogen is found to be reduced to one-half that of the normal, 
gastritis probably exists. The less marked the reduction in the 
zymogen, the more favorable the prognosis. A decided reduction 
or an absence of the zymogen points rather strongly to a severe 
grade of gastritis, which may be accompanied by carcinoma, or 
decided degenerative changes in the gastric, secretory, or glandular 
tissues. 

Chymosin may be present in appreciable or even in nearly 
normal amount in specimens where free hydrochloric acid is 
absent; and it is thought that a step, at least, has been achieved 
in the direction of a cure should free hydrochloric acid appear in 
the gastric contents as the result of treatment. 



PRODUCTS OF GASTRIC DIGESTION. 

Proteid Digestion. — ^According to Nothnagel's "Encyclope- 
dia," the "determination of the different stages of hydration of 
albumin is so far of no practical value. In the first place, the 
method for determining the different intermediary stages in the 
digestion of albumin is too complicated for practical purposes; 
on the other hand, an exact knowledge of these stages is of no 
value to diagnosis. The value of the biuret reaction is certainly 
overestimated." The biuret reaction is a color-test, and is ob- 
tained by adding to the gastric contents an excess of potassium 
hydroxid and treating the mixture, while boihng, with a few 
drops of a I per cent, solution of copper sulphate. In the event 
of peptic digestion having taken place, a peculiar pink or rose- 
reddish color appears (see Biuret Test, page 217). A positive 
biuret reaction indicates that peptic digestion has taken place, 
but does not give us any information as regards the degree of the 
digestion of the albumins. According to Riegel, any gastric 
contents will give a more or less typical biuret reaction, but the 
intensity of this result does not in any way inform us as to the 
strength of the gastric juice. 



PRODUCTS OF GASTRIC DIGESTION. 34I 

Albuminoids. — Among the albuminoids which may be taken 
into the stomach but two of these bodies undergo gastric digestion 
(collagen and elastin), and through this process gelatoses and 
elastoses are formed, while keratin escapes digestion. Collagen 
and elastin do not contribute to the formation of heteroproteoses, 
but protoproteoses and, in turn, deuteroproteoses result, from 
which peptone is eventually obtained. 

Digestion of Carbohydrates. — The gastric secretion is in 
itself unable to digest carbohydrates; but there is evidence sug- 
gestive of the fact that a certain amount of starch is transformed 
into sugar early during gastric digestion. This transformation 
is dependent upon the action of ptyahn, secreted with the saliva 
and taken into the stomach during the ingestion of food. The 
action of ptyalin continues until at least o.oi per cent, of either 
free or combined hydrochloric acid has been secreted. It is to 
be borne in mind that a small quantity of acid inhibits this process, 
since the transformation of starches into sugar is most active in 
neutral or mildly alkahne solutions (see Saliva, page 453). The 
ferment of saliva first converts starch into soluble starch, then 
into erythrodextrin, achroodextrin, and eventually into maltose. 
Where the secretion of hydrochloric acid is abnormally great or 
is continuous, the digestion of starch in the stomach is soon ar- 
rested, and although a sHght digestion of starch may occur, the 
end-products of saccharification are not formed — only the inter- 
mediary products are to be found. On the other hand, where 
the secretion of hydrochloric acid is deficient or absent, a reverse 
condition is observed. 

All-important in analyses for the degree of digestion of starches 
is it to determine whether the end-products of starch digestion 
have been produced, and whether any of the intermediary prod- 
ucts have been generated and are now present, thus indicating 
the degree at which the process of starch digestion was arrested. 

Tests. — The intermediary stages of carbohydrate digestion 
are detected in the following manner: 

Place 10 c.c. of the filtered gastric contents in a test-tube 
and to it add a few drops of Lugol's solution (iodin, o.i part; 
iodid of potassium, 0.2 part; distilled water, 200 parts). With 
this solution starch causes a blue color to appear; erythrodextrin, 
a violet or mahogany brown. Should no color change develop 
upon the addition of Lugol's solution, achroodextrin, dextrose, and 
maltose are present. Soluble starch causes the formation of a 
blackish-blue precipitate with Lugol's solution. 

Achroodextrin possesses a greater affinity for iodin than for 
any other of the intermediary products. It is well to add Lugol's 



342 GASTRIC CONTENTS. 

solution freely in order that some of the intermediary products that 
require large quantities of iodin for the production of the color 
may not escape notice. 

Both maltose and dextrose react with Fehhng's solution and 
are also capable of fermentation. Dextrose reduces Barford's 
reagent: Place a few cubic centimeters of the reagent in a test- 
tube; boil the upper stratum of the liquid, and add to it from 
a pipet a small quantity of the filtered gastric contents. In the 
presence of dextrose a precipitate of red cuprous oxid is formed. 
Barjord^s reagent is composed of a i per cent, solution of acetic 
acid to which a 0.5 to 2 per cent, solution of copper acetate has 
been added. 

Clinical Significance. — In the event of carbohydrate diges- 
tion having been normal in both the mouth and the stomach, 
no color appears upon the addition of the Lugol's solution to the 
gastric contents. The appearance of a violet-blue color upon the 
addition of this reagent signifies that saccharification has been 
incomplete; and it is then necessary to examine further in order 
to determine whether this deficient digestion of carbohydrates be 
due to a deficiency of saUvary ferment, to a hypersecretion of 
hydrochloric acid, or, as is rarely seen, to extraneous causes. 
It is common to find the salivary ferment deficient. 

Digestion of Fat. — It has been demonstrated by Marcet's 
experiments that fats undergo some changes while in the stomach 
— spHtting into glycerin and fatty acids; and it was further 
shown by Ogata and others that the stomach is capable of causing 
a shght disintegration of neutral fats. Again, that from i to 2 
per cent, of oil is decomposed in the normal stomach within a 
period of two hours; and should the oil be allowed to remain 
for a longer period, due to distention of the stomach the result 
of dilatation, a large percentage of oleic acid may be found present, 
reaching a maximum of 6 per cent. The fat-splitting power of the 
stomach is relatively slight, and Riegel's students found that the 
fat-splitting ferment secreted by the stomach is active only upon 
fats that are well emulsified. This ferment is thought to be secreted 
by the mucosae of the fundus. 



FATTY ACIDS. 

Boas and other observers have shown that the formation of 
fatty acids is closely connected with that of lactic acid. Butyric 
acid is at times derived from the lactic acid (Fliigge). This 
change probably depends upon the fact that many, and possibly 
all, the micro-organisms concerned in the production of butyric- 



FATTY ACIDS. 343 

acid fermentation belong to the class of anaerobes. In this con- 
nection it is well to remember that both the Oidium lactis and the 
Bacillus acidi lactici develop in the presence of oxygen. 

Acetic fermentation may occur in the stomach — a process 
supposed to take place in the presence of alcohohc principles. 
This alcohol may not have been introduced into the stomach 
as such, but be the result of acetic-acid fermentation; or, more 
correctly speaking, transformed through the action of the sac- 
charomyces (yeast) upon the sugars ingested. 

Test for Butyric Acid. — Whenever the gastric contents is 
found to contain a large amount of butyric acid, it will emit an 
odor of rancid butter. 

Extract lo c.c. of the gastric fluid with 50 c.c. of ether; evap- 
orate to dryness, and collect the residue with a few cubic centi- 
meters of water. Add a trace of calcium chlorid, and should 
butyric acid be present, it will be precipitated in the form of small, 
oil-Hke globules. This precipitation, consisting apparently of 
oil, will be found to emit a decided odor. 

Test for Acetic Acid. — Extract 10 c.c. of the filtered gastric 
juice with ether, evaporate, and dissolve the residue in a small 
quantity of water. Neutralize cautiously with a weak solution of 
sodium hydrate. In the presence of acetic acid sodium acetate 
is formed. Add to the mixture a few drops (i to 3) of a weak 
solution of perchlorid of iron: acetic acid causes a dark-red color. 
A weak solution of nitrate of silver will also be found to cause a 
rather dense precipitate, but this is readily dissolved upon the ad- 
dition of hot water. 

Quantitative Estimation of Fatty Acids. — The Cahn- 
Mehring method, as modified by McNaught, is as follows: 

1. Ascertain the total acidity of 10 c.c. of the gastric flxuid 
{see page 323). 

2. Place 10 c.c. of the gastric fluid in a beaker or a dish, and 
evaporate over a water-bath to the consistence of syrup; dilute 
with water and subject to titration, as in estimating the total 
acidity. 

Deduct the figure obtained for acidity of the second 10 c.c. 
from that of the total acidity for the first 10 c.c. of filtered gastric 
contents. The difference is equivalent to the amount of fatty 
acids contained in the 10 c.c. of gastric fluid examined. 

Estimation of Organic Acids (Quantitative).— The method 
of Hehner-Seemann depends upon the fact that a quantity of a 
decinormal sodium-hydrate solution, when added to organic acids, 
mixed, evaporated, and incinerated, permits the organic acids 
to be given off as carbon dioxid. Their alkah remains as a car- 



344 GASTRIC CONTENTS. 

bonate. The amount of carbonate is ascertained by titration 
with a y^jj normal solution of hydrochloric acid. 

1. Place 20 c.c. of filtered gastric juice in a beaker and titrate 
\Yith a y^Q normal solution of sodium hydrate. 

2. Eyaporate to dryness and incinerate. Do not continue 
heating after the ash fails to display a radiant flame. 

3. Collect the residue by taking it up with water, then titrate 
with a Y^Q- normal solution of hydrochloric acid. 

Read from the buret the number of cubic centimeters of the 
hydrochloric-acid solution necessary to neutrahze the mixture, 
multiply by 0.00365, and the product will indicate, in terms of 
hydrochloric acid, the amount of fatty acids present in the 20 
c.c. of gastric juice examined. 

Clinical Significance. — Under physiologic conditions fatty 
acids are not present in the gastric fluid except where abnormally 
large quantities of milk and carbohydrates haye been taken. 
Fatty acids are not to be found in normal gastric juice obtained 
after the administration of Boas' test-meal; nor are they likely 
to be found present where there exists chronic gastritis or moderate 
dilatation. Fatty acids are to be obseryed in connection with 
gastric carcinoma. Rarely, butyric acid may be formed in the 
mouth, but from this source the gastric contents seldom displays 
more than a trace of this acid. Again, the gastric contents may 
giye definite reactions for butyric acid after large quantities of 
butter or other fats haye been ingested. Acetic acid is a rather 
rare finding in the gastric contents, but when present and not due 
to the imbibition of alcohol, its significance is practically that of 
butyric acid. 

LACTIC ACID. 

It is generally conceded that the lactic acid found in the 
stomach is the result of bacterial development, such bacteria 
being normally present in the buccal secretions. Again, the gastric 
contents may be found to contain lactic acid during health, but 
in such instances the lactic acid has been introduced into the 
stomach with the food, as was described under Test-meals (page 
315). The bacteria capable of forming lactic acid from carbo- 
hydrates and from sugar are omnipresent in the buccal secretion 
and gastric contents, and induce acid fermentation whenever sugar- 
bearing substances are ingested. 

Granting that a certain amount of lactic acid may be introduced 
with the normal meal or that sugar-charged foods have been taken, 
it is possible for us to find lactic acid in normal gastric contents 
early during the course of digestion. By way of repetition, let 



LACTIC ACID. 345 

it be borne in mind that lactic-acid fermentation is inhibited by 
the secretion of hydrochloric acid, and that this inhibition is 
perceptible even where the amount of hydrochloric acid present 
in the gastric contents is very small. The presence of 0.7 to 1.5 
pro mille of hydrochloric acid, either free or combined, arrests 
the process of the lactic-acid fermentation. It is through this 
physiologic secretion of hydrochloric acid that lactic-acid produc- 
tion is discontinued during the latter stage and height of digestion ;. 
and it is authentically stated that lactic acid does not appear in 
appreciable quantities during the process of normal digestion. 

Lactic acid, even when introduced into the stomach as such, 
may be absent during the latter stage of digestion, and where 
the gastric contents is shown to contain lactic acid early during 
digestion, its disappearance during the latter stage is doubtless 
due to a resorption of the lactic acid ingested. Thus, failure to 
obtain a reaction for lactic acid under such conditions has been 
attributed to the presence of free hydrochloric acid, which pos- 
sibly interferes with the reaction. 

Test for Lactic Acid. — Whenever it is desired to ascertain 
the quantity of lactic acid, it is necessary, first, to introduce the 
stomach-tube and to wash the stomach thoroughly, employing 
from eight to twelve ounces of water; withdraw this water, and in a 
like manner repeat the process several times at a single intro- 
duction of the tube (page 313). In this way any of the lactic acid 
that might be present as a result of stagnant material — a feature 
of gastric dilatation — is removed. Boas' test-meal (page 316) is 
now administered. 

Should there be evidence of stagnation, it may be well to 
cleanse the stomach, as just outhned, in the evening when the 
test-meal is given. Collect the stomach-contents the following 
morning, before any food or water has been taken. 

Caution. — Do not attempt to estimate the lactic acid of the 
gastric contents unless the stomach has been thoroughly washed 
prior to the administration of Boas' test-meal. 

Uffelmann^s Test. — Reagents. — {a) Saturated aqueous solution 
of the sesquichlorid of iron, (h) Concentrated solution of pure 
carbohc acid. 

1. Place 10 c.c. of water in a test-tube, and to it add three drops, 
of solution (a) and three drops of solution (h) ; shake the tube 
gently, when the mixture assumes a bluish-black color. 

2. Add water, shaking thoroughly, until an amethyst-blue 
color results (Plate 23). 

3. Grasp the bottom of the tube between the thumb and index- 
finger, hold in a clear Hght, and add a small quantity of fihered 



346 GASTRIC CONTENTS. 

gastric contents. In the presence of lactic acid the upper stratum 
of the hquid, to which the stomach-contents is added, changes 
to a canary or lemon-yellow color (Plate 23). 

Fallacies. — It is possible to obtain a reaction for lactic acid 
wath Uffelmann's reagent when there is present in the gastric 
contents an abundance of the butyric acid, acid phosphates, 
glucose, and alcohol. Again, lactic acid, when present, does not 
always give a characteristic reaction — the blue changing to gray, 
white, brown, or a dirty yellow, a feature not uncommon where 
the gastric contents is rich in free hydrochloric acid. In fact, 
hydrochloric acid is said to prevent the reaction. These diffi- 
culties are overcome by extracting the gastric contents with ether, 
through which method the presence of o.ooi per cent, of lactic acid 
is detected. 

Place 5 c.c. of filtered gastric fluid in a glass-stoppered sepa- 
rating funnel and to it add 50 c.c. of neutral sulphuric ether, and 
allow it to stand for one-half hour. Then evaporate over a 
water-bath. Take up the residue with 5 c.c. of distilled water, 
and add this mixture to the amethyst-blue solution. 

Kelling's Test. — Place i c.c. of the filtered gastric contents 
in a test-tube and dilute with 9 c.c. of water. The mixture is 
now held in a clear light, and one to three drops of a 5 per cent, 
aqueous solution of the sesquichlorid of iron are added, one drop 
at a time. Lactic acid causes a greenish-yellow color to appear 
upon the addition of the reagent, a feature characteristic of lactic 
acid. 

Boas* Reaction. — Aldehyd is commonly met with in gastric 
fluid, and sarcinae are often found. Tersely, Boas' reaction for 
lactic acid is to recover acetic aldehyd, a substance detectable 
through the employment of Nessler's solution, which is made 
as follows: Dissolve 2 gm. of potassium iodid in 50 c.c. of water, 
and add a variable amount of iodid of mercury, heating until 
only a portion of the mercury remains undissolved. Upon coohng, 
add to the mixture 20 c.c. of water, and place in a glass-stoppered 
bottle. Two parts of this solution are to be added to three parts 
of concentrated potassium hydrate. After the mixture is allowed 
to stand for some time, filter and place in a glass-stoppered bottle. 

Boas' reaction depends upon the fact that the addition of 
aldehyd to Nessler's solution causes a yellowish or reddish pre- 
cipitate, the intensity of such color bearing a direct relation to the 
quantity of aldehyd added. This test is extremely dehcate, 
detecting one part of aldehyd in 40,000 parts of water. 

Procedure. — i. Ascertain the presence or absence of free acids 
by employing the Congo- red test. 



LACTIC ACID. 347 

2. In the presence of free acids add an excess of barium car- 
bonate; evaporate lo c.c. of the filtered gastric contents to a 
syrupy consistence over a water-bath. 

3. Add a few drops of phosphoric acid to the mixture and boil, 
when the carbon dixoid present escapes. 

4. Remove the mixture from the flame, cool, and add to it 
100 c.c. of neutral, alcohol-free ether; after which the mixture 
is shaken at frequent intervals for an hour. 

5. Pour off the ether, evaporate, and take up the residue 
with 45 c.c. of water. 

6. The mixture is now shaken thoroughly, filtered, and 5 c.c. 
of sulphuric acid and a small amount of manganese dioxid are 
added to the filtrate. 

7. Place in an Erlenmeyer flask — a flask closed by a per- 
forated stopper, through which perforation passes a two-hmbed 
glass tube. The longer limb connects with a cylinder into which 
10 c.c. of Nessler's reagent have been placed. The mixture is 
gradually heated to the boihng-point, when aldehyd, resulting 
from the oxidation of lactic acid in the presence of manganese 
dioxid and sulphuric acid, passes over and induces a yellowish-red 
precipitate — aldehyd of mercury. 

Should an alkaline solution of iodopotassic iodid be placed 
in the cylinder instead of Nessler's reagent, iodoform is precipi- 
tated. 

Quantitative Estimation of Lactic Acid. — The principles 
outhned in the preceding qualitative test for lactic acid have been 
appHed by Boas for quantitative analysis. The reader is, there- 
fore, referred to the various steps in the former test while studying 
this method. 

Reagents. — {a) One-tenth normal solution of iodin — 12.65 g^- 
(194.4 gr.), one-tenth of the molecular weight of iodin to the 
hter. 

{h) One-tenth normal solution of sodium thiosulphate — 24.8 
gm. (382.7136 gr.), molecular weight, to the Hter. 

{c) A solution of potassium hydrate — 56 parts of the salt to 
1000 of water. 

{d) Hydrochloric acid, of a specific gravity of 1.018. 

{e) Starch solution: dissolve 5 gm. (77.16 gr.) of starch in 
100 c.c. of warm water. Dissolve 10 gm. (154.32 gr.) of zinc 
chlorid in 100 c.c. of water, and add this mixture to the warm 
starch solution. 

Method. — The reaction is carried out as described under 
Boas' Reaction (page 346, steps 1-6). 

7. Place in an Erlenmeyer flask, the glass stopper of which 



348 GASTRIC CONTENTS. 

is provided with two openings. Through one opening passes 
a bent tube which is connected with the distilhng apparatus. 
The other opening admits a glass tube to which is attached a 
rubber hose, tightly clamped. 

8. Distil until from three-fourths to four-fifths of the mixture 
has passed over, avoiding excessive heat, lest the aldehyd be de- 
composed. 

9. To the distillate add 20 c.c. of a j^ normal iodin solution, 
with w^hich has been mixed 20 c.c. of a potassium hydrate solu- 
tion. Shake this mixture thoroughly, and permit it to stand for 
from five to ten minutes. 

10. The excess of iodin is hberated by adding 20 c.c. of hydro- 
chloric acid; and this excess determined by titration with a yV 
normal solution of sodium thiosulphate. Continue the titration 
until the mixture is nearly decolorized, when add a small quantity 
of the starch mixture and continue the titration until the blue 
color caused by the addition of the starch has entirely disap- 
peared. 

Computation. — Deduct from the number of cubic centimeters 
of the normal solution employed (20) the number of cubic centi- 
meters of the sodium thiosulphate that were required, and this 
difference indicates the number of cubic centimeters of the -^ 
normal solution needed for the formation of iodoform, or the 
amount of lactic acid that was contained in the 10 c.c. of the 
gastric contents examined. 

One cubic centimeter of the y^ normal solution of iodin 
represents 0.003388 gm. of lactic acid; therefore multiply the 
number of cubic centimeters employed by this figure, and the 
product multiplied by 10 equals the percentage of lactic acid 
present. 

Clinical Significance. — Normally appreciable amounts of 
lactic acid are not present in the gastric contents recovered during 
digestion. Lactic acid may be ingested with the food. 

A decided reaction for lactic acid points to diminution or an 
absence of hydrochloric acid (see Clmical SigJiificance 0} Hydro- 
chloric Acid, page 326). 

ACETONE. 

Pathologic gastric fluid may at times contain acetone. This 
finding is evidence favoring primary disease of the stomach or 
intestine, and is not uncommon in gastric cancer. 

Acetone is detected in this situation by the appHcation of 
the Reynolds- Gunning test to the distillate; or the filtrate may 
be tested according to Denning's method (see Urine, page 240)^ 



GASES. 349 



GASES. 



A variable quantity of gas is always found to occupy the 
stomach, and this gas may have been swallowed or may have 
entered the stomach from the duodenum. Again, fermentative 
processes may result in the generation of gases after the hberal 
ingestion of carbohydrates or of fats. During the processes of 
proteid digestion a shght quantity of nitrogen, oxygen, and carbon 
dioxid is to be found in the stomach. Oxygen, when swallowed, 
is for the most part taken up by the blood, in return for which the 
blood gives up carbon dioxid in double quantity. This physio- 
logic feature serves to explain why carbon dioxid is often present 
in large quantities. 

The processes of fermentation concerned in the production 
of both acetic and lactic acids are not capable of forming gas. 
The processes of fermentation interested in the production of 
butyric acid give rise to the formation of hydrogen and carbon 
dioxid. Rarely, under pathologic conditions, marsh-gas results 
from the fermentation of cellulose, but it is questionable whether 
this gas, when present in the stomach, has not gained entrance to 
this viscus from the intestine. The colon bacillus may at times 
be concerned in gas-production. Sulphureted hydrogen may 
result from putrefying albuminates, and its presence is suggestive 
of gastric dilatation, carcinoma, and less often it is found in acute 
gastritis. Gas is absent when lactic acid is present in moderate 
amount. 

Method. — I. Fill a Doremus ureometer with the fresh, un- 
filtered gastric fluid, and place at a temperature of 40° to 45° C. 
(104° to 113° F.) (see Urine, page 194). 

2. When gas-formation has ceased, introduce into the ver- 
tical hmb of the tube a small quantity of concentrated sodium- 
hydrate solution. Should the gas present be carbon dioxid, the 
liquid ascends. 

3. Other gas or gases are estimated from the reading after 
the sodium hydrate has been added. 

4. Sulphureted hydrogen emits its characteristic odor, and 
turns filter-paper that has been moistened with sodium h3^drate 
arnd lead acetate a brown or blackish color. 

Clinical Significance. — Sulphureted hydrogen gas is a not 
uncommon feature of the gastric fluid in gastric dilatation, acute 
gastritis, and gastric cancer. 

Where hydrogen, carbon dioxid, and ammonia are present in 
large quantities, it points to a deficiency of the normal gastric 
secretion. 



350 



GASTRIC CONTENTS. 



MICROSCOPIC STUDY OF THE GASTRIC FLUID. 

Gastric fluid recovered from the stomach apart from the pro- 
cess of digestion will be found to consist, for the most part, of 
mucus and of saliva. Upon microscopic examination, a two- 
third objective being employed, there are usually detected particles 
of undigested food; these particles, when brought into focus 
under a one-sixth objective, will be found to consist largely of 
elastic fibers. Intimately surrounding these particles of tissue 
are to be seen muscle-fibers, fat-droplets, crystals of fatty acids, 
vegetable fibers, starch-granules, leukocytes, mucus-corpuscles, 
epitheHal cells, free nuclei, and granular debris (Fig. 138). 

The stomach-contents may be found to contain epithelial cells 

recovered from the mouth, esoph- 
agus, or stomach, and cells derived 
from the ducts or from the glands 
and supposed goblet-cells are occa- 
sionally found. 

Bacteria. — The bacteria 
present in the gastric contents are, 
as a rule, of no chnical significance; 
yet numerous micro-organisms are 
at times present, among which 
may be mentioned the Leptothrix 
buccalis, various cocci, the sac- 
charomyces. Bacillus subtiHs, and 
the Boas-Oppler bacillus. 

The Boas-Oppler bacillus is 
quite constantly present in the 
gastric contents during the course of gastric carcinoma. This 
bacillus (Fig. 137) appears in long, segmented chains, which 
often assume a somewhat tortuous course; stains readily with the 
ordinary anihn dyes, and is not motile. This bacillus is found 
present in the gastric contents where free hydrochloric acid is 
diminished or absent, and where lactic acid abounds. The 
question has arisen as to whether or not the Boas-Oppler bacillus 
is concerned in the production of lactic acid. It is not uncom- 
mon to find rather dense aggregations and clumps of these bacilli 
disseminated throughout the gastric contents. 

Clinical Sipiificance. — They are fairly constant in gastric 
fluid whenever lactic acid is plentiful, but they have not been 
shown to be concerned in the etiology of gastric carcinoma. 

Sarcinae Ventriculi. — These organisms occur in the gastric 
contents and are arranged in squares or packets ; they are to be 




Fig. 137.— Boas-Oppler bacillus from 
near top of fluid from washing in case 
of gastric cancer. Observation at Penn- 
sylvania Hospital. 



MICROSCOPIC STUDY OF THE GASTRIC FLUID. 



351 



seen scattered throughout the gastric contents, and when studied 
singly, they resemble somewhat a miniature bale of cotton 

(Fig. 138). 

Clinical Significance. — The gastric contents may be found to 
contain few sarcinae during heakh. They are also found early 
during carcinoma, and in pyloric carcinoma where there is yet 
a secretion of hydrochloric acid. Sarcinae are seldom observed 
in advanced gastric carcinoma. Their presence in the gastric 
fluid is suggestive of a distinct variety of fermentation, yet they 
are by no means constant where gastric fermentation exists. 

Bile. — The vomit may often be stained with bile, and upon 




Fig. 138.— stomach-contents : i, 2, Saieiua; ventriculi ; 3, yeast; 4, needles of fatty acids; 
5, fat-droplets ; 6, starch-granules (Riegel). 

microscopic examination such vomit is likely to display crystals 
of cholesterin, leucin, tyrosin, and biliary pigments. The micro- 
chemic reactions for the determination of these substances have 
been described in the Chapter on Urine (page 239). 

_ Tissues. — Many writers have described in detail the finding 
of shreds of tissue, particles of tumors, etc., recovered through 
the stomach-tube, and such portions of tumors or sloughing 
ulcers are of great diagnostic value when thus obtained. In case 
the piece of tissue be very small, it is well to place a portion of it 
upon a skde, tease thoroughly with a needle, and then mount 
in water, applying rather firm pressure to the cover-glass. In 



352 GASTRIC CONTENTS. 

this way it is often possible to secure a rather satisfactory specimen, 
which in the case of sloughing gastric cancer may be composed 
largely of epithehal cells and will display the features common 
to cancer. If there be sufficient tissue recovered, it should be 
hardened and studied in sections (see works on pathology). 

It is also possible, though rare, to recover shreds of mucous 
membrane from cases of chronic gastritis and from neurasthenic 
individuals. Such tissue, whenever recovered, must, of course, 
be studied microscopically, and careful note be made as to the 
presence or absence of nests of cancer-cells, etc. A fact ever to 
be borne in mind is that gastric carcinoma may exist, and at 
the same time there be a shght sloughing of the mucous mem- 
brane elsewhere. It is not possible, therefore, to exclude the 
presence of cancer where tissues recovered are not found to be 
cancerous. Again, tissue that has been subjected to the action 
of the gastric juice for some time is unfit for microscopic study. 
In my own experience it has been extremely rare to recover par- 
ticles of tissue from the stom.ach-wall, and I do not recall a single 
instance where a diagnosis was attained through the study of 
such particles of tissue. 

THE VOMIT, 

Odor. — Normal gastric juice has a characteristic odor, which, 
while it resembles that of acids, is unlike any other well-known 
odor. Pathologic gastric fluid may emit an odor, due to the 
presence of certain gases previously described (page 349). A 
putrid odor is suggestive of pyloric stenosis, with or without ulcera- 
tion of the gastric surface. Following the ingestion of certain 
foods, the gastric contents will be found to display the odor 
known to such foods. The odor of ammonia is emitted by the 
gastric contents of uremic persons, and after the administration 
of toxic doses of phosphorus the gastric fluid will give off an odor 
of garhc. Carbohc acid also lends its odor to the vomit. 

The vomit will vary greatly, depending upon the conditions 
by which it is excited; the preexist ence of nausea; the material 
taken in the stomach prior to vomiting, and whether or not the 
vomit contains bile, saliva, mucus, blood, or fecal material. 
Again, material may seemingly be vomited which, in reality, is 
simply regurgitated from the esophagus. 

Vomiting may occur immediately after the ingestion of food, 
some hours after taking food, or upon rising; which influences 
materially alter the character of the vomit. Large quantities of 
undigested food may be vomited two or more hours after the in- 
gestion of a meal, but this observation is rare and occurs in cir- 



THE VOMIT. 



353 



rhosis of the stomach. There is at times a regurgitation of food, 
mucus, and saKva where stricture of the esophagus or of the 
cardiac portion of the stomach exists, but such regurgitation, as 
a rule, occurs soon after the taking of food. It is not uncommon, 
however, to find food regurgitated some days after it has been 
taken — a condition seen most often in gastric dilatation. Food 
regurgitated from the esophagus is distinguished from that ejected 
from the stomach by the fact that the latter may contain gastric 
juice and biliary coloring-matter. During the course of gastric 
neuroses, ulcer, acute gastritis, and early in chronic gastritis, as 




Fig. 139.— Vomited material : a, Muscular fiber; b, white blood-corpuscles; c, c\ c" , flat 
and cylindric epithelia ; d, starch-corpuscles ; e, fat-globules ; J\ Sarcinae ventriculi ; ^, yeast 
ferment ; h, i, cocci and bacilli (those near h were once found by von Jaksch in a case of ileus, 
hence arising from intestine); k, fat-needles, connective tissue ; /, vegetable cells (von Jaksch). 



well as in reflex (spinal) vomit, the food is rather thoroughly 
digested. 

Where the nausea precedes the vomiting, the vomitus will be 
found to contain a large quantity of mucus and of saliva. It is, 
therefore, unsafe to form any deductions concerning the amount 
of mucus found in vomited material. 

Saliva. — Persons suffering from chronic catarrhal conditions 
of tlie throat may at times vomit almost pure saliva. Reactions 
for saliva are to be obtained in almost any vomit, and may be 
detected through the methods outlined under Saliva (see page 
452). 

Mucus. — The presence of mucus in the vomit is of little 
consequence, but where the gastric contents is obtained through 
23 



354 GASTRIC CONTENTS. 

the stomach-tube, large quantities of mucus are to be seen only 
in pathologic conditions, and are commonly suggestive of the 
existence of mucous gastritis. It has been claimed that where the 
gastric contents is purely mucus, gastric dilatation exists. Large 
amounts of mucus may at times collect in the stomach between 
the stages of digestion, but this condition is certainly rare. In 
addition to the characteristic appearance which mucus lends to 
the gastric contents, it will be found to react characteristically 
with acetic acid (see Urine, page 262). 

Bile. — The vomit is commonly colored, due to the presence 
of bile, but it is unusual to find bile in the gastric contents that 
has been recovered through the stomach-tube, and I recall but 
a single instance, that of a neurasthenic female of thirty-five years. 

Biliary vomit, when frequent, points to the existence of ob- 
struction to the lower duodenum or upper portion of the jejunum. 
The presence of bile in the gastric fluid is in a measure indicative 
of pancreatic disease. 

Stercoraceous Vomit. — Stercoraceous material, when vom- 
ited, is at once recognized by its odor (fecal). It is found to 
contain phenol, indol, and skatol (see Feces, page 366). Bile and bile 
acids may also be present in the fecal vomit, which is, as a rule, 
alkaline in reaction and occurs in intestinal obstruction. 

Blood. — The vomit may contain blood in a number of con- 
ditions, many of which induce secondary gastric hemorrhage. 
Among the primary causes of gastric hemorrhage and the vomiting 
of the blood are : gastric cancer, ulcer, traumatism, the retching 
of vomiting, and acute gastritis. It is also found secondary to 
chronic Bright's disease, valvular heart disease where compen- 
sation has been lost, chronic lung disease, cirrhosis of the liver, 
anemia (pernicious anemia, leukemia, and chlorosis), and, rarely, 
it is the result of vicarious menstruation. 

Detection. — Should the blood be present in large quantities, 
it will be found to lend its color to the vomit, such color 
varying in intensity from that of a dirty-brown to a blackish 
hue. This color may be largely due to the action of the gastric 
juice upon the blood. It is often possible to detect blood-cor- 
puscles upon microscopic examination of the gastric fluid. 

Minute quantities of blood, when present in the gastric juice, 
are best detected through the method suggested by Miiller and 
Weber: Treat 10 c.c of gastric contents with about 2 c.c. of 
ether, shaking to effect a mixture. The ether will be found to 
separate into a clear stratum when the mixture is allowed to stand 
for a few minutes; should this separation fail to occur, add a 
few drops of alcohol. The addition of ether causes, in the pres- 



THE VOMIT. 355 

ence of blood-pigment, a brownish-red color to develop, which 
is dependent upon acetate of hematin. Bile-pigment causes a 
yellowish-brown color. The guaiacum test (page 31) should 
also be appHed to the ethereal extract. Spectroscopic study, 
however, is scarcely practical. 

Klunge's Aloin Test. — Dissolve as much aloin as will rest 
on the tip of an ordinary spatula in 10 c.c. of 70 per cent, 
alcohol. 

1. Treat the gastric fluid or feces as directed by Miiller and 
Weber, except pour away the ether when it collects at the top 
after the first treatment. 

2. Place 2 c.c. of the ethereal extract in a test-tube and to it 
add 2 c.c. of the aloin reagent. Add drop by drop, shaking after 
each addition, ten to twenty drops of Merck's oil of turpentine. 

3. Stand aside for a few minutes, when should blood be present 
the lower half of the liquid becomes a rich cherry-red color. In 
the absence of blood a violet color develops. 

Clinical Significance. — In cancer of the stomach a positive reac- 
tion is obtained with both gastric fluid and with feces. Benign 
gastric and duodenal tumors and gastric ulcer show an intermittent 
positive reaction with the feces. Negative results are obtained 
with the feces in cases of gastritis acidi, hyperacidity, neuroses and 
benign dilatation. 

Pus. — It has not been my privilege to detect pus in the gastric 
contents obtained through the stomach-tube. It is to be detected, 
however, in cases of diphtheric gastritis, in gastric carcinoma 
located at the fundus and lesser curvature, and, according to 
certain authors, the recovery of a dram or more of pus through 
the stomach-tube is of diagnostic value in this disease; but should 
a large quantity of pus be obtained, it would doubtless have gained 
access to the stomach through a fistulous opening, and might 
come from the diaphragm, fiver, pleura, lung, or any of the ad- 
jacent viscera. 

Pus is distinguished by its microscopic appearance. 

Parasites. — I have found the ascaris, oxyuris, and segments 
of the tape-worm in the vomit. Other observers have detected 
the ankylostomum, trichinae, and, according to Simon, the Tricho- 
monas vaginalis has been found present in the vomit from a case 
of esophageal cancer. 



CHAPTER IV. 
THE FECES. 

By an examination of the feces we are able to determine the 
character of this discharge, and to draw certain conclusions as 
to the nature of intestinal digestion or of any derangements that 
may be present; provided that these derangements are accom- 
panied by abnormahties in either the physical or the chemic 
properties of the feces. At times the feces may contain definite 
products of disease, or the pathogenic organisms of disease may 
be present: for example, the intestinal animal parasites and the 
organisms producing dysentery. 

It is impossible to obtain much cHnical evidence from the 
study of the feces, because we are dealing with the last step of an 
extremely tedious and compHcated process, the exact nature of 
the previous steps of which is not yet thoroughly understood. 
It is, therefore, possible for a shght pathologic variation to exist 
in the feces, and for this variation to escape our notice. Again, 
the feces may vary within wide Hmits during health, as to both 
their physical and their chemic properties, and this fact renders 
it extremely difficult to draw well-balanced deductions, except 
in connection with a few maladies. The bulk of the feces will 
be found to consist of undigested particles of food and of un- 
absorbed secretions furnished by the various glands that empty 
into the gastro-intestinal canal, to which may be added a variable 
amount of mucus, epithehal cells, and bacteria. 

COLLECTION OF THE FECES. 

It is preferable to have the feces passed into a well-warmed 
pan or vessel, w^hich should be sent to the laboratory as soon 
as possible, so that the specimen does not become chilled. It is 
of especial importance that the specimen be kept warm when we 
are searching for the Amoeba coli or any other motile animal 
parasite. Should the specimen be collected from a patient at 
his residence, it should be passed into a warm vessel, as previously 
stated, and whenever a portion of the feces is desired for clinical 
study, this should be placed in a wide-mouthed bottle, which should 

356 



FECES IN HEALTH AND DISEASE. 357 

be corked tightly and kept as warm as possible while being carried 
to the laboratory. As soon as the specimen is received in the 
laboratory, the tightly corked bottle should be placed in an irf- 
cubator at a temperature of 37° C. (98.6° F.), where it should be 
kept until the time for its examination. 



GENERAL CHARACTERS OF THE FECES DURING HEALTH 
AND DURING DISEASE. 

Frequency. — The frequency of the intestinal discharges will 
be found to vary considerably in the adult. Children upon a 
milk diet usually have three or four evacuations of the bowel 
daily. Adults and children upon sohd food have, as a rule, one 
or two stools in twenty- four hours. There are certain individuals 
who may have three, or even four, movements daily, and, on the 
other hand, it is not unusual to find persons who have a movement 
of the bowels only once or twice a week. In one case under 
personal observation the patient claimed that he had a rather 
large stool once in every eight days. This man was sixty-four 
years of age, a surveyor by occupation, and, from his occupation, 
was constantly walking over the mountains of the eastern United 
States. He died of pneumonia at the age of sixty-four years, his 
final illness being the first time he had called on a physician for 
professional services. 

Pathologic Frequency. — Pathologic constipation may re- 
sult from a variety of diseases; but, in a general way, maladies 
beginning abruptly are accompanied by constipation, except 
cholera and cholera morbus. In typhoid fever and in dysentery, 
in which frequent stools are characteristic, the diarrhea is pre- 
ceded by constipation. It is impossible to say that any person 
is suffering either from diarrhea or from constipation unless the 
physician is acquainted with the normal number of bowel move- 
ments for the given individual. The quantity of material dis- 
charged at each movement is hkely materially to influence the 
number of the discharges. For example, in acute dysentery 
the number of movements may vary from 20 to 200, or even more, 
daily, but the quantity discharged at each operation is extremely 
small and may not exceed one dram. The character and the 
quantity of the food taken will also be found to influence materially 
the frequency and the quantity of the intestinal discharges. The 
grade of the peristalsis also influences the number of stools — 
rapid peristalsis exciting frequent bowel movements, while slug- 
gish peristaltic waves favor obstipation. Interference with the 
lumen of the intestinal canal, from whatever cause, induces con- 



358 THE FECES. 

stipation or obstruction, depending upon the degree to which 
the cahber of the intestine is reduced. 

Clinical Significance. — Diarrhea, when present, is signifi- 
cant of intestinal catarrh. Such an inflammatory process of 
the intestine may be the result of errors in diet, exposure to cold, 
or the growth of some infectious agent: e. g., Bacillus typhosus. 
Amoeba coH, Bacillus dysenteriae. Whatever the cause, it is to 
be remembered that the lesions involve the mucosa of the large 
intestine. 

The stools are always thin, more or less watery, and in cer- 
tain diseases they have some characteristic features: e. g., the pea- 
soup stool of typhoid fever, and the mucoserous and mucosero- 
purulent stools of acute dysentery. These stools may occur every 
few hours or more frequently. The stools of Asiatic cholera are 
characterized by their rice-water appearance. The Hquid portion 
of such stools is derived from the patient's blood-serum. 

Drugs. — Drugs may also excite frequent bowel movements, 
and may at times cause a true intestinal catarrh. In such a con- 
dition the stools closely resemble those of acute dysentery. 

Constipation. — Obstinate constipation, while it is extremely 
troublesome and annoying, may not be of serious moment. It 
is an early and valuable diagnostic sign of peritonitis and paral- 
ysis of the intestine. It is further suggestive of stenosis of the 
intestine, fecal impaction, or complete obstruction of the bowel. 
Constipation with the passage of ribbon-Hke stools points def- 
initely to a progressive lessening of the lumen of the intestine. 

In amebic dysentery there may be constipation which alter- 
nates with exacerbations of diarrhea — six to twelve movements 
daily. It is impossible to draw any universal conclusions concern- 
ing the various degrees of constipation, since each case is prac- 
tically a law unto itself. Constipation may form a prominent 
feature of esophageal carcinoma and of mahgnant disease of the 
stomach or the intestine. In such cases it is usually the result 
of starvation. 

Amount. — Under normal conditions the amount of feces 
dejected during twenty- four hours will be found to vary between 60 
and 250 gm., an average of from 100 to 200 gm. The wide degree 
of fluctuation is directly influenced by the quantity and the char- 
acter of the food ingested, the degree of intestinal irritation, and 
the frequency of the peristaltic waves. Under pathologic condi- 
tions it is not unusual to find from 500 to 1200 gm. of excreta 
discharged daily. Protracted constipation or a temporary in- 
testinal obstruction may be followed by a copious discharge of 
feces. 



FECES IN HEALTH AND DISEASE. 359 

Form. — In health the stool is rather firm or mushy, its con- 
sistence depending directly upon the quantity of water which 
it contains, and this quantity of Hquid is hkewise governed by 
the character of the food and the quantity of the hquids ingested. 
When the patient is placed upon a vegetable diet, the stools will 
be found to contain about 80 per cent, of water; when upon a 
mixed diet, the quantity of water present is somewhat lessened; 
and when the diet is formed principally of animal proteids, the 
dejecta may contain not more than 60 per cent, of water. 

Scybalous masses are seldom observed under normal con- 
ditions, but are commonly seen in the bowel movements some 
hours before the development of diarrhea. Thin, tape-like or 
ribbon-hke stools are often indicative of rectal stenosis (see Con- 
stipation, page 358). 

If a stool is permitted to stand in a vessel for some time, the 
watery element occupies the upper stratum, while the solid con- 
stituents are thrown down as a precipitate. Such stools are 
characteristic of intestinal catarrh, and are best seen during 
typhoid fever, although this condition may be observed whenever 
the feces are composed largely of water. It is to be remembered 
that such a pecuharity may be favored by the admixture of urine. 

Odor. — The odor of the stools may be somewhat character- 
istic of the disease affecting the alimentary tract, or it may be 
altered by the food or by medicines (onions, asafetida) that have 
been taken. As a rule, the odor is dependent upon indol and 
skatol present in the feces, although at times a decided odor of 
sulphureted hydrogen may be detected, and, rarely, the odor of 
methane or of phosphin. 

Pathologic Odor. — The following alterations in the odor of 
the stools have been noted during pathologic conditions. In 
persons suffering from acute or protracted alcohoHsm the odor 
of the stools is extremely foul. The dejecta of children, when 
acid fermentation has been going on in the intestinal tract, often 
emit the odor of fatty acids. When alkahne fermentation has 
taken place in the presence of albuminous material, the stools 
may have a putrid odor. The admixture of blood and pus with 
the feces may produce a rather heavy odor, resembling that of 
rancid butter. The feces will be found to give off an am- 
moniacal odor when a fistulous communication with the blad- 
der permits the escape of urine into the bowel. Cadaver-like 
smelHng stools are characteristic of gangrenous processes along 
the ahmentary tract, usually affecting the large bowel. In cases 
of Asiatic cholera the stools emit a spermy odor which is probably 
due to the presence of cadaverin. In cases of tuberculous ulcera- 



360 THE FECES. 

tion of the bowel a decidedly foul odor is present. In acute 
catarrhal dysentery, when there are frequent stools composed of a 
small quantity of mucus, blood, and pus, there may be no odor 
to the feces, but there is usually an escape of a large amount of 
fetid gas with each fecal discharge. In a case of amebic dysen- 
tery under personal observation the feces had a sweetish odor. 

Color of Stools. — Under normal conditions the color of the 
feces will be found to vary, in accordance with the character of 
the food taken, from a light yellow to a brownish black or blackish 
blue. Usually the more soHd the consistence of the feces, the 
darker the color, except w^hen the excessive color is directly depen- 
dent upon the food taken. Exposure to the air and light causes 
the stools to become darker than they were when passed. In 
health, huckleberries produce blackish stools; chocolate gives 
the feces a dull-gray color; cocoa produces a Hght-gray shade; 
chlorophyl colors them green; and starches produce a yellow 
color; fats, too, cause a clay color. 

Hemorrhage. — After hemorrhage from the bowel the feces 
may be blood-red in color; but when the blood has gradually 
oozed into the bowel for a long period, the stools become black, 
on account of the formation of hematin. In other cases hemor- 
rhage from the stomach, from typhoid ulceration, or from other 
forms of intestinal lesion is followed by deep black stools, from 
the formation of sulphid of iron. When the hemorrhage is 
rather profuse, — say a few ounces of blood, — the stools are tar- 
like in color and in consistence. As a rule, the higher in the 
ahmentary tract the seat of the hemorrhage, the darker the color 
of the feces; thus, coffee- colored stools are seen after gastric and 
duodenal hemorrhages. Fresh blood, when adherent to scybalous 
masses or to soHd feces, is usually from the rectum and anus. 

Tests for Blood. — In case it is impossible to detect blood- 
ceUs in the feces by the microscope, one must resort to the special 
chemic tests for the presence of blood-pigments. Such chnical 
observation is, however, more scientific than practical in value. 
Minimum quantities of blood, when present in the feces, may be 
detected by the method suggested by JMiiller and Weber (see 
Gastric Contents, page 354, and Blood, p. 31). 

Karczynski-Jaworski Test. — i. Place a small amount of the 
feces in a porcelain dish, add a smaller amount of potassium 
chlorate, and one drop of hydrochloric acid (c. p.). 

2. Heat carefully over the flame of a Bunsen burner until 
the mixture is decolorized (the addition of one or more drops of 
hydrochloric acid may be required). During this process chlorin 
escapes. 



FECES IN HEALTH AND DISEASE. 36 1 

3. Add from one to five drops of a dilute solution of potassium 
ferrocyanid; the appearance of a distinct Prussian-blue color 
indicates the presence of blood-pigment. 

Fallacies. — Pus, when present in the feces in appreciable 
amount, will produce the same reaction with potassium fer- 
rocyanid. See also Klunge's Aloin Test, p. 355. 

Drugs. — The various preparations of iron, bismuth, and 
manganese dioxid, when administered by the mouth, produce 
a dark-brown or black color of the feces. This color is dependent 
upon the formation of sulphids of these metals. The stools 
assume a decidedly greenish hue after the administration of 
calomel, which is probably due to an excess of biliverdin in the 
intestine. Ipecac produces clay-colored stools; while senna and 
santonin, when administered in physiologic doses, give a yellow 
color to the feces. 

Bilious Stools.— The so-called "bihous stools" vary in 
color from bright yellow to dark green. This color is due to the 
escape of unchanged or but slightly altered bile which has passed 
hurriedly through the bowel. Such feces may be filtered, and the 
filtrate tested for the presence of bile (see Urine, pa-ge 239). When 
the bile-supply is cut off from the intestine, the feces soon become of 
a clay color and have a pecuhar ghstening appearance. This ghs- 
tening appearance of the feces is doubtless due, in a measure, to 
the lack of bile; but to a certain extent it is caused by the small 
particles of fat that are more or less thoroughly disseminated 
throughout the mass, not having been absorbed by the intestine. 

Clay-colored Stools. — Clay-colored stools are found in 
conjunction with all forms of obstructive jaundice (see Fatty 
Stools); but the feces from a patient with obstructive jaundice 
have a hght-brown color if the patient is kept upon a diet containing 
a minimum amount of fat. 

It has been proved that the lack of color of the feces is not 
always due to the absence of bile nor to the presence of fats; 
and it is, therefore, supposed that the decomposition of urobiHn 
may result in the formation of decolorizing products. Nencki 
has described a substance which he called " leukourobilin " ; and 
it is possible that some allied product or products are concerned 
in decolorization of the feces. 

Green stools may be due to the development of the Bacillus 
pyocyaneus or other bacteria which form a green chromogen. 
There is some reason for beHeving that the feces may at times 
owe their color, in part at least, to the development of other 
chromogenic bacteria. 

Red Stools. — Carter and MacMun have reported three 



362 THE FECES. 

instances in which the feces turned red upon exposure to the air 
and hght. It is suggested by the latter of these writers that the 
chromogen here concerned is closely allied to stercobilin. In 
this connection it may be profitable to cite a series of experiments 
conducted at the Philadelphia Hospital in collaboration with 
Dr. Charles A. Ohver, and reported by the latter.* These 
experiments showed that the chromogens resulting from the 
development of the different chromogenic bacteria produced a 
different shade, and often an entirely different color, when grown 
under colored glass plates: e. g., red, green, blue, and yellow. 
When kept in the dark, Httle or no color develops. I am inchned 
to beheve that feces that become red on exposure to the Hght owe 
this redness to the chromogens of bacterial development — BaciUus 
prodigiosus, Micrococcus prodigiosus, etc. 

CHEMISTRY OF THE FECES, 

In American laboratories there appears to be but a small 
amount of time devoted to the study of the chemistry of the feces. 
Sufficient has been done, however, to permit of definite deduc- 
tions regarding the chemistry of normal feces; but the data are 
by far too small to justify conclusions regarding the chemistry 
of the feces in disease. 

REACTION OF THE STOOLS. 

The reaction of the stools of a normal adult is, as a rule, 
alkaline; but it is sometimes neutral and occasionally acid. The 
alkalinity of the normal feces is dependent upon ammoniacal 
fermentation. The acidity is due to the presence of lactic or of 
butyric acid, the formation of either of w^hich may occur, by 
fermentation, in the intestine. The feces of children when taking 
a milk diet should, under normal conditions, give a shghtly acid 
reaction. 

Clinical Significance. — In the adult, whenever the feces are 
decidedly acid, the reaction is indicative of intestinal catarrh with 
the production of lactic- and butyric-acid fermentation in the 
intestine. When the feces of children are found to be highly 
acid, the existence of an intestinal catarrh may be inferred; and 
in the adult the acidity depends upon acid fermentation. A 
decided alkaline reaction may depend upon the occurrence of 
alkahne fermentation; it is usually indicated by its characteristic 
odor (see Odor, page 359). The reaction of the feces is of 
limited diagnostic value. 

*"Amer. Jour. Med. Sci.," April, 1902. 



COMPOSITION OF THE FECES. 363 



COMPOSITION OF THE FECES. 

Dunglison credits Simon with the following as the composi- 
tion of normal feces: 

Water 77.3 per cent. 

Mucin 2.3 

Proteids 5.4 

Extractives 1.8 

Fats 1.5 

Salts 1.8 

Resinous, biliary, and coloring-matters 5.2 

Insoluble residue of food 4.7 

Gautier gives the following table regarding the composition 
of the freshly passed feces (Gautier's estimations are based upon 
1000 parts by weight) : 

Adult Man. Suckling. 

Water 733-oo 851.3 

Solids 267.00 148.7 

Total organic material 208.75 i37-i — including 54 parts of 

Total mineral material io-95* i3-6 mucin, epithelium, 

Alimentary residue 83.00 and calcareous salts. 

The organic material yielded: 

Man. Suckling. 

Aqueous extract 53-4° 53-5 

Alcoholic extract 41-65 8.2 

Ethereal extract 30-7o 17-6 — of which 2.2 is choles- 

terin. 

In a general way it is possible to gain a fairly clear, concise, 
and at the same time general idea of the feces by considering under 
the following headings the various chemic constituents present: 

1. Unassimilated Food. — Probably the greater portion of 
the sohd and semisolid materials of the feces consists of food 
that has not been assimilated, but which, if taken in proper 
amounts into a stomach during health, should have been assimi- 
lated. This class of food-material appears in the feces oftenest 
as a result of overeating. These food-materials consist for the 
most part of starches, albuminous materials, and fats. 

2. Indigestible Matter. — ^A varying proportion of the feces 
will be composed of substances not capable of digestion, and 
hence incapable of assimilation; among which class are to be 
found gums, resins, gelatinous substances, chlorophyl, pigments, 
nucleins, and the various insoluble salts. 

3. Substances from the Digestive Tract. — A portion of the feces 
will be seen to consist of organic substance derived from the 
gastro-intestinal tract and from the adjacent glands which empty 

* Not comprising earthy phosphates. 



364 THE lECES. 

their secretions into the intestine, such as epithehal cells, mucus, 
bile acids in various stages of transformation, cholesterin, and 
lecithin. 

4. The feces also contain substances practically ready for ab- 
sorption, but which, owing to peristaltic movements, have been 
hastened through the bowel before such absorption could take 
place; these are emulsified fats, fatty acids, biHary acids, and 
leucin. 

5. Products oj Metabolism . — A variable amount of the feces 
is dependent upon metabohsm, such metabohc products being 
ehminated through the alimentary tract. In this connection urea, 
uric acid, and the various xanthin bases should be considered,, 
although these substances are not eliminated by the feces in 
amounts sufficient to warrant their special study in this excretion. 

6. Piirin Bodies. — For description see page 533. 

7. Coloring-matter. — A small amount of coloring-matter is also 
found in the feces. It consists of the modified pigments of the 
blood and of the bile — hematin, stercobilin, and hydrobihrubin. 
Hematoidin, pure blood, and the unaltered bile-pigments are ab- 
normal constituents of the feces. 

8. Decomposition Products. — The products of decomposition 
dependent upon bacterial development, such as the various fatt^ 
acids, butyric and isobutyric acid, lactic acid, amido-acids, acid 
amids, leucin, tyrosin, phenyl-acetic acid, phenol, skatol, excretin, 
indol, and cresol, are constituents of the feces. Both ammonium 
carbonate and ammonium sulphid are produced by processes of 
decomposition. 

9. Gases. — The gases present in the feces during health vary in 
direct proportion to the character of the food ingested. The for- 
mation of gas may be a feature of certain diseases. Under normal 
conditions carbon dioxid, hydrogen, nitrogen, and marsh-gas ap- 
pear in the feces. The carbon dioxid present is dependent upon 
alcoholic fermentation, butyric-acid fermentation, and upon the 
putrefaction of albumins which take place within the intestine. 
Theoretically, carbon dioxid is supposed to pass directly from the 
blood into the intestine. 

Nitrogen may be swallowed, but a portion of this gas found in 
the feces is probably evolved from putrefying albumins. Glucose, 
while undergoing fermentation, generates a certain percentage of 
marsh-gas. 

It is reasonable to suppose that a special study of the gases of 
the feces may enable one to form an approximate idea of the putre- 
factive and fermentative changes taking place in the intestinal 
tract ; but as yet a practical clinical method for the quantitative and 
qualitative detection of such gases has not been proposed. 



TYROSIN. 



365 



I shall consider briefly the chemistry of the biHary acids, the 
pigments, the fatty acids, and cholesterin, and shall mention cer- 
tain other substances known to occur in normal feces. Bloody 
stools have been discussed under a separate heading. 

TYROSIN. 

Tyrosin is conceded to be the mother-substance of phenol, 
indol, skatol, and cresol. Tyrosin, when present in the gastro- 
intestinal tract, is the result of the putrefaction of albumins. 




Fig. 140.— Distilling apparatus. 



It is readily destroyed in the intestinal tract after it is produced, 
with the formation of phenol, indol, skatol, and cresol, which may 
be found in the feces. Tyrosin itself is rarely found in this ex- 
cretion (see Urine, page 268). Phenol, indol, skatol, and cresol 
may be detected in the feces by the following reactions: 

Method of Detection. — i. The feces should first be well 
diluted with water, acidified with phosphoric acid, and then 
distilled. By this process all the volatile fatty acids, indol, skatol, 
phenol, and cresol will be forced into the distillate. 

2. Neutralize the distillate with sodium carbonate and distil 



366 THE FECES. 

again. During this second distillation the fatty acids are left be- 
hind as sodium salts, while indol, skatol, phenol, and cresol pass 
into the receiver. 

3. Phenol may be separated from indol, skatol, and cresol by 
rendering the second distillate alkaline with potassium hydroxid 
and redistilling. During this third distillation indol, skatol, and 
cresol pass over, while phenol is left behind. /According to Mar- 
shall, this precipitate is tribromphenolbrom or tribromobrom- 
phenol. 

4. The residue in the retort should be distilled with sulphuric 
acid, and pure phenol will be forced over in the distillate, as may 
be shown by the following reactions: 

Phenol. — (a) Place a portion of the distillate in a test-tube and 
add a few drops of a solution of iron perchlorid. In the presence 
of phenol an amethyst-blue color develops (see Tests jor Lactic 
Acid, page 345). 

(h) Place a few cubic centimeters of the distillate in a test-tube 
and add an equal volume of bromin water. In the presence of 
phenol a crystalline precipitate of tribromphenol is formed. 

(c) The distillate, when treated with Millon's reagent (see 
Urine, page 217), shows a decided red color when phenol is pres- 
ent, due to the formation of acid nitrate of mercury. 

Indol. — In order to separate indol from skatol it is necessary to 
observe their degrees of solubility closely. Small plates of indol 
are liquefied at 52° C. (125.6° F.). They are also readily soluble 
in hot water, alcohol, and ether. During this process the mixture 
will be found to emit a feculent odor. 

(a) Indol, when treated with nitric acid and a variable amount 
of sodium nitrate, gives a red, crystalhne precipitate of nitrosoindol 
nitrate. 

{h) Take a small piece of a clean pine stick and moisten it with 
an alcoholic solution of indol; then plunge the stick into a solution 
of hydrochloric acid. The wood will change to a cherry-red color 
if indol be present. 

Skatol. — {a) Crystalhne skatol appears in quite regular plates 
which dissolve at a temperature of 95° C. (203° F.). Crystals of 
skatol are less readily soluble than are crystals of indol; but during 
their solution a similar feculent odor is given off. 

{h) Skatol, when treated with nitric acid and sodium nitrate^ 
results in an opalescent (milky) mixture. 

{c) Skatol, when boiled with nitric acid (sp. gr. 1.2), gives the 
xanthoproteic reaction. 

{d) The color reaction of hydrochloric acid and pine wood 
previously dipped in a solution of skatol is different from that pro- 



FATTY ACIDS. 



367 



duced by hydrochloric acid and pine wood dipped in a sohition of 
indol. First moisten the wood with a weak alcohoHc solution of 
skatol, and then dip it into a strong solution of hydrochloric acid; 
a cherry-red color, which soon changes to blue or violet, will be 
produced. 

FATTY ACIDS. 

All members of the group of fatty acids, from formic acid to 
stearic acid, may at times be found in the feces. 

Derivation. — While a portion of these fatty acids is derived 
from the fats ingested, it is to be remembered that some of them 
are derived from the ingested carbohydrates and proteids. 

Physical Properties of Fatty Acids.— The fatty acids are 
monobasic, and are soluble in water, alcohol, and ether. The 
alkaline salts of the fatty acids are also soluble in water and in 
alcohol, but are not soluble in ether. The silver salts of the fatty 
acids are not readily soluble. 

Detection. — i. The reader is referred to the special method 
described under Tyrosin for 
the detection of phenol, indol, 
skatol, and cresol. If the first 
distillate obtained from dis- 
tillation of the feces be neu- 
tralized with sodium carbon- 
ate and distilled a second 
time, the fatty acids remain 
in the retort as their sodium 
salts. 

2. Evaporate this solution over a water-bath (Fig. 141) to dry- 
ness, and extract the residue with alcohol; evaporate the alcohol, 
and dissolve the residue in water. By this method a solution is 
obtained that may be employed for the further study of the fatty 
acids. 

Whenever it is desired to separate the different fatty acids, the 
majority of authors recommend converting them into silver or 
barium salts, which may be distinguished by their solubility in 
water. It is possible, however, to employ fractional distillation 
for the separation of fatty acids. 

Formic Acid. — Formic acid is a colorless, pungent liquid 
which boils at 100° C. (212° F.). To a concentrated solution of 
the alkaline salts of formic acid add silver nitrate. Upon the ap- 
plication of heat a black precipitate results; but if the mixture be 
allowed to stand at room-temperature for a time, the silver salt 
blackens without the application of heat. 




Warm-water bath. 



368 THE TECES. 

Place a neutral solution of formic acid in a test-tube and add a 
few drops of a solution of iron perchlorid. A blood-red color in- 
dicates the presence of formic acid. When this red mixture is 
heated, its color fades, and finally disappears on boiling. At the 
same time a rusty-colored precipitate collects at the bottom of the 
tube. 

Acetic Acid. — Acetic acid is a colorless liquid, of a penetrating, 
vinegar-Hke odor, boihng at a temperature of 119° C. (246.2° F.). 

1. Acetic acid when cautiously neutralized gives a blood-red 
color after the addition of a few drops of iron perchlorid. 

2. A neutral solution of the alkaline salts of acetic acid gives a 
precipitate when treated with silver nitrate. This precipitate is 
soluble in hot water, but reduction does not take place. 

Butyric Acid. — Butyric acid is an oily substance having an 
odor like that of rancid butter, and boiling at a temperature of 
137° C. (278.6° F.). 

1. Solutions of butyric acid and of its salts do not turn red when 
treated with iron perchlorid. 

2. Solutions containing the alkaline salts of butyric acid, when 
treated with silver nitrate, give a precipitate which is insoluble in 
cold water. 

3. Solutions containing the salts of butyric acid emit its char- 
acteristic odor upon the addition of acids. 

Valerianic Acid. — Valerianic acid is an oily hquid having a 
pungent odor and boiling at a temperature of 176.3° C. (349.3° F.). 
Its odor, while disagreeable, can scarcely be said to be character- 
istic. When treated with solutions of silver nitrate, its silver salts 
crystallize in rather regular plates which are not readily soluble. 

Propionic Acid. — Propionic acid is a sour, pungent, oily sub- 
stance, boiling at a temperature of 117° C. (242.6° F.), When 
treated with a dilute solution of iron perchlorid, it does not produce 
a red color. When treated with silver nitrate, it is practically 
indistinguishable from formic acid. 

BILIARY ACIDS. 

Among the bihary acids found in the feces are glycocholic acid, 
taurocholic acid, and cholalic acid. Glycocholic acid (C26H^3NOg) 
and taurocholic acid (CogH^jNSO-) are normal constituents of the 
bile, and are converted into cholalic acid {C^fi^fi.^ and glycocoll, 
or cholalic-acid taurin, by processes of decomposition. Cholalic 
acid is the biliary acid found in the feces, because it is the product 
of the decomposition of glycocholic and taurocholic acids in the 
intestinal canal. 



PIGMENTS OF THE FECES. 369 

Detection. — The detection of biliary acids in the feces can be 
accomphshed only after phenol, indol, skatol, cresol, and the fatty 
acids have been removed by distillation with phosphoric acid 
(see Test for these substances). 

1. After removing the previously named substances from the 
feces, dissolve the residue with water; boil and filter. 

2. Treat the filtrate with lead acetate and a small quantity of 
ammonium hydroxid until a precipitate forms. This precipitate 
contains the biliary salts of lead. 

3. Wash the precipitate with water, and boil with alcohol to 
remove the salts of the biliary acids; filter. 

4. Treat the final filtrate with sodium carbonate, in order that 
the lead salts may be transformed into sodium salts; filter again, 
evaporate this filtrate to dryness, and extract the residue with hot 
alcohol. The salts of the biliary acids may crystalhze, but the 
rule is to obtain an amorphous, dirty, brownish precipitate. 

5. Treat this amorphous precipitate with ether, so as to pro- 
duce crystalhne substances. Crystallization of the amorphous 
precipitate is not necessary, however, since it is possible to employ 
this material for further testing. 

Pettenkofer's Test. — (a) Place a small amount of the amor- 
phous precipitate in a dish, and add sufficient water to dis- 
solve it completely. To this solution add two-thirds its volume 
of concentrated sulphuric acid; the temperature of the mixture 
should not be above 70° C. (158° F.). 

{h) While the mixture is kept warm, add a 10 per cent, solution 
of saccharose drop by drop. In the presence of biliary acids the 
entire mixture assumes a beautiful red color which changes to blue 
or violet on standing. 

PIGMENTS OF THE FECES. 

Stercobihn and hydrobilirubin deserve special mention in con- 
nection with the pigments of normal feces. According to Gau- 
tier, stercobilin, which is the principal coloring-matter found in the 
feces, is derived from bilirubin. According to the reports of a 
number of chemists, stercobihn and hydrobilirubin appear to be 
similar, if not identical. 

Detection. — Extract the feces with acid alcohol, and to this 
extract add water and a variable quantity of chloroform. Upon 
vigorous shaking, the pigment dissolves. 

Stercobihn, upon treatment with zinc chlorid and ammonium 
hydroxid, gives four absorption-bands. Hydrobihrubin, in strik- 
ing distinction, gives but three absorption-bands when subjected 
24 



370 THE FECES. 

to this treatment (see Spectroscopy, page 43). It will be found 
of interest to compare the spectra of stercobilin, normal urobilin, 
and hydrobihrubin. The last is probably identical with the so- 
called febrile urobilin. 

CHOLESTERIN. 

A trace of cholesterin (C26H^^O) is to be found in practically 
all the body-fluids. The method of the production of cholesterin 
wherever it may appear is undetermined. 

Crystals. — Crystals of cholesterin (Fig. 92) appear as thin, 
colorless, semitransparent plates, one or more margins of which 
are usually irregular, showing a more or less jagged, imperfect, 
saw-like edge. The remainder of the margins are usually clearly 
cut and of regular outhne. Crystals of cholesterin are, as a 
rule, irregularly oblong or square. Crystals from which one 
corner appears to have been broken are also common. Crystals 
of cholesterin may occur singly, but it is more common to find 
them in dense aggregations. 

Solubility. — Crystals of cholesterin are soluble in water, dilute 
acids, and alkahs. They are freely soluble in boiling alcohol, 
ether, chloroform, and benzol. After solution in hot alcohol 
cholesterin is precipitated on cooling. 

In the feces the cholesterin does not appear in crystalline form 
except under rare conditions. 

Detection. — i. In order to detect cholesterin in the feces the 
fatty acids, phenol, indol, skatol, and cresol must first be removed 
by distillation (see Special Study of these substances). 

2. Next add sulphuric acid to the residue; extract with alcohol, 
and continue the extraction with ether. 

3. Filter the ethereal extract, remove the ether by distillation, 
and then treat the residue with sodium carbonate, thereby con- 
verting any fatty acids present into their sodium salts, 

4. Evaporate the mixture to dryness and extract with ether. 

5. Filter the previously prepared alcoholic extract, and then 
supersaturate the filtrate with sodium carbonate; remove the alco- 
hol by distillation ; dissolve the residue in water, and continue the 
extraction with ether. By this process any bile acids, oleic acid, 
stearic acid, etc., separated by further analysis, may be converted 
into their respective barium salts (see Fatty Acids, page 367). 

6. Cholesterin and the fats are dissolved in the ether. Place 
this final solution in a beaker and evaporate over a water-bath; 
treat the residue with an alcoholic solution of potassium hydroxid. 

7. Evaporate this alcoholic solution over a water-bath (Fig. 
141), dilute the remaining fluid with water, and extract with ether. 



MACROSCOPIC AND MICROSCOPIC CONSTITUENTS. 371 

All fats present will be found suspended in the aqueous solution 
as soaps. The cholesterin, on the other hand, will have been dis- 
solved in the other. 

(a) Place the suspected solution on a slide, add a drop of water, 
apply a cover-glass, and examine with a one-fifth or one-sixth 
objective. Crystals of cholesterin (Fig. 92), if present, may be 
readily seen. Add a drop of concentrated sulphuric acid to the 
edge of the cover-glass, and observe closely the changes that take 
place. The crystals fade gradually, and their once rather distinct 
margins are changed to a yellowish or reddish color. 

(b) Place crystals of cholesterin in a test-tube; add chloroform 
and a concentrated solution of sulphuric acid; shake vigorously for 
one-half minute. If cholesterin be present, the chloroform will be 
changed to a purphsh-red or blood-red color. The layer of sul- 
phuric acid becomes highly fluorescent. 



MACROSCOPIC AND MICROSCOPIC CONSTITUENTS. 

Particles of Food, etc. — Normal feces contain particles of un- 
digested food and of solid materials that have been taken with the 
food. The network of vegetable cells is often seen, as well as 
distorted muscle-fibers of a faint yellow color and elastic fibers. 
The elastic fibers are of a clear, pearl-white shade, and even when 
shghtly colored are distinguishable by the fact that they are well 
outhned and often present in apparent double contour. Starch- 
granules and small, flake-like particles of casein are also found in 
the normal feces. Muscle-fibers may be detected in every speci- 
men of feces when the patient has been on a diet rich in meats. 
The number of these fibers present will depend upon the individ- 
ual, the degree of mastication, the amount of meat ingested, and 
the thoroughness with which digestion has been accomplished. 

It is not uncommon to find some muscle-fibers that have re- 
tained their characteristic outhnes and others that show slight 
distortion; but most of the muscle tissue taken as food is so 
broken up that it cannot be recognized, or else is represented 
by small, disc-hke, yellowish fragments. It is only after careful 
study that one is able to recognize these latter particles as 
partly digested muscle tissue. The most characteristic features of 
such particles are, first, their parallel outhnes, and, second, their 
characteristic cross-striations, both of which features are best seen 
with a one-sixth or one-eighth objective (Fig. 142). 

Clinical Significance. — A large number of connective- tissue 
fibers in the feces is conclusive evidence that digestion has not 



372 



THE FECES. 



been completed, and is due either to a pathologic condition of the 
gastro-intestinal tract or to decided errors in diet. 

Starch. — Starch-granules and chlorophyl are found in some 
of the undigested vegetable foods, but it is uncommon to find free 
starch-granules in normal feces, unless the patient has been fed 
upon food composed principally of starch. Starch-granules are, 
therefore, rather common in the feces of children who are fed upon 
prepared foods. 

Under pathologic conditions it is not uncommon to find iso- 
lated starch-granules in the feces, as well as undigested particles 
of vegetable matter in which starch-cells are to be seen. 

Detection. — A portion of the feces examined under the micro- 







X 



rs 



Fig. 142. — General view of the feces: a. Epithelial cells and leukocytes; b, stone-cells; 
c, cuticular formations; d, crystals of ammoniomagnesium phosphate; e, fat-crystals; /", 
yeast-fungi ; g-. Amoeba coli ; h. Trichomonas intestinalis ; z, Cercomonas intestinalis ; ni, ovum 
of ascaris ; n, ovum of oxyuris ; o, ovum of trichocephalus ; />, ovum of ankylostomum ; ^, 
ovum of bothriocephalus ; r, ovum of Taenia saginata ; j, ovum of Taenia solium (Jakob). 



scope should be treated with Lugol's iodin solution by placing a 
drop of this solution at the margin of the cover-glass, so that it 
gradually comes in contact with the specimen. Starch-granules, 
upon coming in contact with 'the iodin solution, change to blue. 

Mucoid, Serous, and Bloody Stools. — Mucus, when it is dis- 
tinctly recognized in the stools, is indicative of a catarrhal inflam- 
mation of the mucous membrane of the intestine, yet this finding 
alone should not be regarded as one of serious moment, since it may 
occur in conjunction with but slight intestinal inflammation. There 
is normally a certain amount of mucus secreted by the intestine, 
and small particles of mucus may be seen clinging to the surface of 
firm stools. Large quantities and thick shreds or rope-Hke masses 



MACROSCOPIC AND MICROSCOPIC CONSTITUENTS. 373 

of mucus are suggestive of catarrh of the large intestine (Fig. 
143), and in such a catarrhal condition rounded, sago-like gran- 
ules of mucus are often found. Such bodies are seen in the rice- 
water stools of cholera ; they are also found in the acute catarrhal 
conditions. Scybalous masses may also be coated with mucus, 
indicating a chronic intestinal catarrh. 

The discharge of mucus is abundant in the feces in cases of 
acute intestinal catarrh whenever the large intestine is involved 
in the process, and in nearly all cases of catarrhal dysentery. 

Microscopically, it is uncommon to find small particles of mu- 
cus in pathologic feces, but these may be present without carrying 
any chnical significance. Should such particles of mucus show 
evidence of bile-staining, they are indicative of catarrh of the 
small intestine. Numerous microscopic particles of unstained 
mucus are generally conceded to be suggestive of the existence of 
a catarrhal process high in the large intestine or in the lower sec- 
tion of the small intestine. 

Caution. — Whenever the feces contain many small particles 
of mucus, it is well to test for starch by adding a drop of iodin so- 
lution. 

Casts of the Bowel. — Mucus cylinders are at times passed with 
the dejecta. These may be mere shreds of mucus-like material or 
they may form a complete cast of the bowel. Such casts usually 
have a constant diameter throughout their entire length, and their 
free surfaces will be seen by the naked eye to be studded with fine 
white granules. When the inflammatory process is acute, their 
surfaces may be streaked with blood. Cylinders of the bowel 
may vary in length from two to sixteen inches in catarrhal 
enteritis. In the case of a woman studied in my clinic at the 
Howard Hospital, a cast from four to ten feet in length was 
passed at intervals of from ten days to two weeks. In the case 
of a child of three years recently under my observation, a mucous 
cast of the bowel was passed daily for a period of one week, each 
cast varying from ten to eighteen inches in length. 

In cases of diphtheritic dysentery true casts of the bowel are 
passed with the feces. They are, as a rule, but a few inches in 
length, and are usually only partial casts of the intestine. Diph- 
theric casts of the bowel are much darker in color than mucous 
casts, and when studied microscopically, are seen to be formed of 
a true diphtheric membrane. 

Microscopic Study. — Microscopically, these mucous casts are 
found to consist principally of a faintly opalescent, hazy, homo- 
geneous material (mucus). A number of epithelial cells, leuko- 
cytes, red blood-cells, mucus-corpuscles, and Charcot-Leyden 



374 



THE FECES. 



crystals appear to be entangled in this mucus-like substance. 
Other crystals are rarely seen. When the catarrhal process has 
gone on to the stage of necrosis of the epithelial cells lining the 
intestine, a true diphtheric membrane is formed which is much 
thicker than the mucous cast and contains necrotic material. 

Clinical Significance. — Mucous casts of the bowel are found 
in connection with both chronic and acute inflammation of the 
intestinal mucosa. Their pathologic significance depends upon 
the numbers of epithelial cells which they contain, because the 
presence of these cells serves as a direct index of the degree of de- 
struction that is taking place in the bowel. Mucous casts are not 
uncommon in gastroptosis and in enteroptosis. 




Fig. 143. — Portion of cast from bowel, observed at Howard Hospital (obj. Spencer one-sixth). 



In primary diphtheric dysentery the passage of a large number 
of diphtheric casts with a considerable amount of blood is usually 
followed by death within the course of a few hours. 

Secondary diphtheric dysentery, which usually develops late 
during the course of some chronic malady, — e. g., diabetes, tuber- 
culosis, etc., — may persist over a long period of time, during which 
both long and short, rather pale casts of the bowel may be passed. 

Epithelial Cells. — Under normal conditions but few epithelial 
cells are to be found in the feces, and, in fact, epithehal cells do 
not concern us from a practical standpoint except there be some 
inflammatory process of the intestinal mucosa. 



MACROSCOPIC AND MICROSCOPIC CONSTITUENTS. 375 

It is not unusual, however, to find rather well-preserved cylin- 
dric (goblet) cells. Indeed, all the varieties of cells known to 
develop upon mucous surfaces are occasionally met with in the 
normal feces. When the epithelial cells have been separated 
from the mucous membrane for some time, they become distorted, 
probably because water is extracted from them. 

The epithelial cells, when killed en masse, may be thrown off 
in the form of the bowel casts which have been previously described. 
In acute inflammatory processes the intestinal epithelial cells may 
appear in the feces in great numbers, a feature common to ca- 
tarrhal dysentery. When the stools are decidedly watery, the epi- 
thelial cells appear rolled together, giving the liquid an appearance 
as though particles of cracked rice were floating in it. Again, other 
epithelial cells may be found more or less closely connected with 
shreds of mucus, and such cells at times show evidence of 
degeneration. Bile-stained epithelial cells are supposed to 
indicate a lesion of the small intestine. Cylindric and goblet- 
cells are not infrequently found in the dejecta of dysentery. 
Large clusters of epithehal cells have been reported as occurring 
in the feces of individuals suft'ering from carcinomatous disease 
of the rectum. 

Blood-corpuscles. — It is unusual to find unaltered red blood- 
cells in the feces except when an ulceration involving either the 
lower portion of the colon or the rectum exists. In acute catar- 
rhal dysentery mucobloody discharges are common, and in them 
the erythrocytes may be but slightly altered. It is to be borne in 
mind that the feces may be markedly colored with blood, and yet 
microscopic study will fail to reveal the presence of red blood-cells. 
It is impossible to recognize the red blood-cells as such in the feces 
when a hemorrhage has occurred high in the intestine, but instead 
of blood-cells, the feces will contain small, roundish, amorphous 
masses of a brown-red color which consist, in part at least, of 
hematoidin. Crystals of hematoidin are occasionally met with in 
the feces after intestinal hemorrhage (see Plate 17), but in such a 
condition crystalline hematoidin appears, for the most part, in the 
form of rhombic plates. In my own experience, I have been un- 
able to find red corpuscles in the feces after a hemorrhage during 
the course of typhoid fever. In this condition the higher the 
seat of the hemorrhage, the more likely is one to find crystals of 
hematoidin and the darker in color will be the feces. 

Leukocytes. — The appearance of a small number of leukocytes 
in the feces is of no practical clinical moment, but when leuko- 
cytes are present in abundance, they are suggestive of an inflam- 



376 THE FECES. 

matory process, either catarrhal or ulcerative, which affects the in> 
testinal mucous membrane. The number of leukocytes present 
in the feces is in direct relation to the degree and character of the 
lesion. 

Pus. — Pure pus is seldom recovered from the feces; but when 
it is found, it indicates that an abscess has probably communicated 
with the bowel. 

In acute catarrhal dysentery the feces are seen to contain blood, 
mucus, and a large quantity of pus. I have repeatedly seen muco- 
purulent and seropurulent stools in this disease, and it is not un- 
common for the pus to form a large proportion of the entire stool, 
but it is extremely rare to find purulent stools devoid of serum, 
mucus, and blood. I have in mind the case of a woman, recently 
under observation, in which from one and one-half to three ounces 
of pure pus escaped with the daily stool. It is unusual to find 
blood in such stools, and they seldom contain mucus in appre- 
ciable amount. In conditions of this nature one is certainly 
not warranted in regarding such quantities of pus as being of 
intestinal origin. In the case just cited, for example, the clinical 
manifestations of catarrhal enteritis were wanting. 



INTESTINAL CONCRETIONS. 

Biliary. — The importance of the examination of the feces for 
the presence of biliary concretions is, doubtless, sufiiciently em- 
phasized by works in both medicine and surgery. It is a diagnos- 
tic method which should be employed whenever abdominal pains 
of an obscure or questionable nature or true hepatic colic exists. 

Method of Detection. — (i) Collect every bowel movement for 
from twenty-four to forty-eight hours following an exacerbation 
of colic. (2) Direct that each stool be passed into a rather large 
commode. (3) Add to the stool one gallon of water, and stir 
thoroughly; allow the mixture to stand for a short time, and pour 
off the supernatant liquid. (4) i\gain add water, and stir to effect 
a perfect mixture. (5) Cut a piece of surgeon's gauze large enough 
to cover the top of a second vessel, and tie it to the rim of the top of 
the vessel with string or fasten with adhesive plaster. 

The mixture of feces and water is now poured upon the gauze^ 
which acts as a filter and separates any calculi that may be pres- 
ent. In this manner calculi may be readily detected. When 
found, they should be placed in a bottle and hermetically sealed, 
since nearlv all gall-stones deteriorate upon exposure to air and 
light.^ 

Biliary concretions vary in size from that of a grain of sand to 



INTESTINAL CONCRETIONS. 377 

that of a small olive. They are usually of a dark-yellowish, green- 
ish, or black color. The composition of the calculi varies greatly : 
those, for example, consisting for the most part of biliary pigments 
will be brown in color, and will be found to sink in water. Chemi- 
cally, such calculi may contain lime-salts and salts of copper and 
zinc. It is the rule to find calcuh composed of calcium salts to 
be distorted and irregular in outline. Again, hepatic calculi may 
be composed exclusively of cholesterin, in which case they are 
soft and light in color, varying from white to a faint green shade. 
Cholesterin calculi are best distinguished by the fact that they are 
lighter than water. 

It is reasonable to believe that every hepatic calculus consists of 
a nucleus, and this nucleus is often found to be composed of phos- 
phates, and less frequently of sulphates. Joseph McFarland was 
the first one to recover a pure culture of the Bacillus coli communis 
from the nucleus of a gall-stone. Since his observation Welch 
and other observers have detected, in addition to the Bacillus coli 
communis, the Bacillus typhosus, in the nuclei of gall-stones. 
When it is desired that the exact composition of a gall-stone be 
ascertained, it will be found necessary to subject it to chemic an- 
alysis. 

Intestinal Calculi. — It is exceptional to find intestinal concre- 
tions passed with the feces; but when such concretions are dis- 
covered in the stools, it is supposed they have been formed in the 
saccules of the colon or in the appendix. It is further supposed 
that the calculi result from the accumulation of calcium and mag- 
nesium salts upon solid particles which have probably been in- 
gested and which have served as an appropriate nucleus for their 
development. Such calculi may form in the folds of the rectum, 
yet their usual seat of origin is in the cecum. 

Intestinal Sand. — A singular case of intestinal sand was 
reported by Duckworth and Garrod,* who contribute an inter- 
esting paper upon the subject of true enteric lithiasis. I have 
been able to find reports of three other cases in the literature. The 
stools in the case cited by the above authors consisted of a vari- 
able amount of loose brown material which was found to con- 
tain about a teaspoonful of gritty sand. This sand was soluble 
in boiling nitric acid, but insoluble in cold liquor potassas. It is 
of interest to note that the colon and the sigmoid flexure were 
readily palpable in Duckworth and Garrod's case. These authors 
suggest that there are true and false intestinal sands, the former 
consisting of organic material, the latter, of remnants of vegetable 
food. 

*" Lancet," March 8, 1902. 



378 THE FECES. 

Dr. John K. Mitchell * has reported the case of a male, aged 
forty, from whom a quantity of intestinal sand was recovered. 
Dr. Mitchell tells me he has seen three additional cases where sand 
was passed vvdth the feces. He further states that all these cases 
were upon a milk diet at the same time when such sand was passed. 

Fatty Stools. — Under normal conditions the feces contain a 
variable amount of fat, either in the form of oil-droplets — highly 
refractile polygonal masses which vary in color from yellowish- 
white to dark yellow or red — or as needle-like crystals (see Crys- 
tals 0} Feces, below). Pathologic fat is usually recognized by the 
glistening, greasy appearance of the stool, which is often of a gray- 
ish-yellow color. When fat is present in large amounts, the feces 
are clay-colored and sometimes nearly white (it is not essential that 
the bile-duct be obstructed in order that the stools be white or clay- 
colored). Feces in which there is much fat become softer and 
develop a glistening appearance when slightly heated. A portion of 
fatty feces when placed under a one-sixth objective will show at least 
one, and probably all, of the above-named forms in which fat m^ay 
appear. It is not infrequent, however, to find only the yellowish 
masses present, in which case add a drop of concentrated sul- 
phuric acid to the margin of the cover-glass, remove the slide from 
the microscope, and heat it gently. This treatment will cause the 
masses of fat to break up and form oil-droplets. Whenever fat is 
found, it is stained black with a solution of osmic acid and pink with 
an alcoholic solution of Sudan III. 

Clinical Significance. — Fat appears in the stools after the 
ingestion of large quantities of fat ; during the course of diseases 
accompanied with progressive emaciation; and in the anemias, 
both primary and secondary. In such conditions the quantity 
of fat present in the stool is not large, as a rule. In all forms of 
obstructive jaundice the feces will be found to contain an abnor- 
mally large amount of fat. Fats are also found in the feces of 
persons suffering from pancreatic disease, and during the course 
of acute infectious fevers. 



CRYSTALS OF THE FECES. 

Crystals are among the commoner constituents of the feces, 
appearing in fairly large numbers under normal conditions. Cer- 
tain crystalline bodies may be found in the feces of special maladies 
(see Bloody and Fatty Stools). 

Fatty Acids. — Crystals of the fatty acids, when present in 
the feces, appear in the form of slender needles which are often 

* "Trans. Phila. Col. Physicians," 1903. 



CRYSTALS OF THE FECES. 379 

arranged in rather dense aggregations, forming more or less perfect 
rosets (Fig. 97). These crystals are regarded by Gerhardt as 
consisting of calcium and magnesium salts of the higher fatty 
acids. Other observers have thought them to be crystals of tyro- 
sin. Feces containing crystals of the higher fatty acids also con- 
tain crystals of calcium and magnesium soaps (Fig. 97), which 
have been described in the Chapter on Urine (page 266). 

Clinical Significance. — Crystals of fatty acids, when abund- 
ant in the feces, point directly toward an impediment to 
the absorption of fats and also to some intestinal derangement. 
In all forms of obstructive jaundice crystals of the fatty acids 
are abundant in the feces. They are a normal constituent of 
the feces of children during the nursing period, and may be found 
in moderate amounts during childhood. 

Charcot-Leyden Crystals.— Charcot-Leyden crystals (Fig. 
181) may be found in normal stools and are to be seen in such 
febrile conditions as typhoid fever, dysentery, etc. 

Following infection with a variety of intestinal parasites the 
feces may contain Charcot-Leyden crystals, as has been observed 
in connection with ankylostomiasis. They are found with 
less frequency in cases of tape-worm infection, and it has been 
stated that they do not occur in the feces during an infection 
with the dwarf tape- worm (Hymenolepis nana). They are also 
found with oxyuris, lumbricoid, and trichocephalus infections. 

Charcot-Leyden crystals have been found in large numbers 
in the feces of amebic dysentery. My own experience has been 
that when the feces are sufficiently diluted, the finding of Charcot- 
Leyden crystals is the rule. When present in great numbers, 
they appear as dense aggregations. 

Cholesterin. — Cholesterin is a normal constituent of the feces, 
although it usually appears in some form other than that of the 
characteristic plates (page 92). 

Hematoidin. — Crystalline hematoidin appears in the feces 
whenever gastro-intestinal hemorrhage has occurred. The num- 
ber of crystals present is usually in direct relation with the quantity 
of blood that has escaped into the bowel. Their number is also 
influenced by the site of the hemorrhage: the smallest number 
is found in the feces when the hemorrhage comes from the 
rectum (see Bloody Stools, page 372). 

Phosphates. — The organic salts of lime are not infrequently 
found in the feces, and crystalline calcium phosphate may appear 
in dense clusters. Crystals of triple phosphate (ammonium, mag- 
nesium, and calcium) are also a normal constituent of the feces; 
they have been described in connection with the urine (page 275). 



380 THE FECES. 

Bismuth. — Following the administration of large doses of 
bismuth subnitrate or of bismuth salicylate the feces may contain 
blackish crystals which shghtly resemble crystals of hemin. These 
are crystals of bismuth sulphid. 



BACTERIA. 

All suspicious- looking particles should be removed from the feces 
by means of a needle and placed in a Petri dish, or probably a better 
procedure is to smear them thinly upon a slide, fix by heat, and 
stain. When the object is to study living parasites and to ascer- 
tain the general microscopic character of the feces, it is wtII to 
place the suspicious particle in the center of a shde, add one or 
more drops of water to it, and allow a cover-glass to fall gently 
upon the mixture. A specimen thus prepared may be studied under 
a one-sixth, one-eighth, or even an oil-immersion objective, so 
that the various bacteria and animal parasites, including amebae, 
may be readily seen. The specimen often becomes chilled during 
the process of preparation, and then the Amoeba coli, should it 
be present, would assume a spheric shape and become quiescent. 
Upon gently warming one extremity of the slide, however, the 
Amoeba coli will assume decided motility, and may be seen 
retracting and throwing out pseudopodia in various directions. 
Motile bacteria also become active when thus warmed. 

Care must be taken not to make the slide too hot while en- 
deavoring to bring out the motility of organisms. A warm stage 
may be obtained for the microscope, and this will be found to 
prolong materially the life of the parasites found in the feces. 

Tubercle Bacilli. — The detection of the tubercle bacillus in 
the feces is readily accomplished whenever ulceration of the in- 
testine, due to the development of this organism, exists. Collect 
a small portion of the purulent or mucoid material from the 
feces, smear it thinly upon a glass slide, and stain it for the tubercle 
bacillus, as directed in the Chapter on Sputum (page 438). It 
is of special importance that when acid-resisting bacilli are found 
in the feces, they be carefully stained to dift'erentiate between the 
tubercle bacillus and the other so-called acid-fast bacilli (page 
441). When the feces have been allowed to stand for some 
hours, I have found that the condensation liquid that collects 
above the sediment of the feces often shows many tubercle 
bacilli; but this finding is by no means constant. Again, I have 
repeatedly examined the feces of persons suffering from tuber- 
culous ulceration of the intestine in which it was impossible to 
find tubercle bacilli; yet these same individuals were found at 



BACTERIA. 381 

postmortem to have extensive ulcerations of the intestines which 
were tuberculous in nature. 

Clinical Significance. — Tubercle bacilli, when found in 
the feces, point conclusively to the existence of tuberculous ulcera- 
tion of the intestines. 

Pus-producing Organisms. — The feces always contain a 
great number of bacteria, the majority of which are non-patho- 
genic, but at times we find pus-producing organisms present in 
the feces, particularly in the dejecta of patients with acute dysen- 
tery or diphtheric dysentery. Streptococci, staphylococci, and 
bacilli are usually found in such cases. It is impossible to deter- 
mine, merely from the staining properties of these organisms, 
which of them is of pathogenic importance. It, therefore, becomes 
necessar}" to make cultural studies of the bacteria found in the 
feces in cases of pathologic conditions of the intestines. Such 
cultural studies must be carried to the point at which the different 
organisms present are isolated. It is also necessary to make 
animal experiments in order to estimate the degree of patho- 
genicity possessed by any one organism recovered. 

The typhoid bacillus may be recovered from the stools during 
the ulcerative stage of typhoid fever, but this method of study is 
more of scientific than of practical value, since the Widal reaction 
furnishes the most valuable clinical datum concerning this dis- 
ease. The isolation of the Bacillus typhosus from the stools is a 
complicated and tedious process. 

The bacillus of .Shiga may be recovered from the dejecta of 
persons suffering from acute catarrhal dysentery, but this finding 
is much more constant in tropic and subtropic regions than it is 
in temperate climates. The bacillus of Shiga, when isolated 
from the feces of acute dysentery, will be found to agglutinate 
with the patient's serum (see Serum-diagnosis, page 116). 

It is not within the scope of this volume to describe in detail 
the cultural characteristics of the various bacteria encountered in 
clinical diagnosis; but in view of the fact that bacillary dysentery 
has received special study by a number of investigators, among 
whom should be mentioned Krause, of Germany, Deycke, of 
Turkey, Froch von Drigalski and Conradi, of Prussia, and Flex- 
ner,* Duval, Vedder, and Mason, of the United States, and more 
recently by Duval and Basset, who have isolated this bacillus 
from the dejecta in summer diarrhea of infants, it appears war- 
rantable to insert the morphologic and general cultural character- 
istics of Shiga's bacillus. 

The bacillus of Shiga is a small, slender rod with somewhat 

* "Phila. Med. Jour.," Sept. i, 1900, p. 414. 



382 THE FECES. 

rounded ends. Morphologically, it resembles the typhoid bacillus 
and the colon bacillus, to which group of bacilli it probably 
belongs. The bacillus is slightly motile, stains with the ordinary 
anihn dyes, and is decolorized by Gram's method. When specially 
cultivated and stained, it is furnished with flagella. The bacillus 
may be isolated from the feces during the first few days of the 
disease, but is not readily found during the subacute and chronic 
stages of dysentery. 

"The value of bacillary diagnosis is lessened by the fact that 
the bacilli cannot often be found in the early stages or in mild 
cases of the disease, but when the morbid process is low down in 
the colon or in the rectum, they can generally be found without 
difficulty."* From the fifth to the seventh days of the disease 
the bacilli are abundant in the blood and mucus of the dejecta; 
but with the establishment of convalescence, the bacilli lessen in 
number and finally disappear, to reappear with the occurrence 
of relapses. 

Isolation of Shiga's Bacillus. — The practical operation of 
isolating the bacillus of Shiga from the feces is as follows : 

1. Tubes containing agar-agar are placed in a glass containing 
water that has been warmed to melt the medium. When the 
agar-agar is melted, it is inoculated with the mucous or the 
bloody portion of the stool. 

2. The necessary care is to be employed, and the liquid agar- 
agar is poured into a Petri dish and placed in a cool place until 
the agar- agar has solidified. The dish is then placed in an incu- 
bator at a temperature of 37° C. (98.6° F.). 

3. At the end of from twelve to twenty-four hours the dish is 
examined and cultures made from the isolated colonies of bacilli 
that have developed upon the surface of the agar-agar. 

4. The cultures of bacilli and cocci are separated by the mere 
smearing of a slide with a portion of the colony, and staining 
to determine the morphology of the organism present. After 
determining which of the colonies contain bacilli only, the different 
forms of bacilli are then separated — "the practical operation of 
separating the different kinds of bacilli which grew in the plates 
was to inoculate glucose agar-agar stab-tubes from the different 
colonies" (Flexner). 

5. Place these stab-cultures in the incubator at a temperature 
of 37° C. (98.6° F.) for twenty-four hours. At the end of this 
time those containing the colon bacillus and other gas-producing- 
organisms will show evidence of gas-formation. Those tubes in 
which no gas has been evolved are probably inoculated with the 

* C. F. Mason, "Jour. Amer. Med. Ass.," July 23, 1903, p. 243. 



ANIMAL PARASITES OF THE FECES. 383 

bacillus of Shiga, and should be further studied to determine its 
identity. 

Mason states that "if agglutinating reaction is positive" with 
the patient's blood-serum; if no gas is produced and milk is not 
coagulated, the micro-organism is the Bacillus dysenteriae. 

Shiga advances the following valid reasons for believing that 
this bacillus is the exciting cause of dysentery: 

1. It may be cultivated from the feces in all cases. 

2. It is not to be found in other disease or in health. 

3. The number of bacilli present in the feces bears a direct 
relation to the intensity of the existing morbid process. 

4. It is present in the lesions in the intestinal wall. 

5. It agglutinates only with the blood of persons suffering 
from bacillary dysentery; and this agglutinative power is said to 
increase with the approach of and during convalescence. 

6. A pure culture of the Bacillus dysenteriae (Shiga) was in- 
tentionally given to a condemned criminal, who developed the 
disease. Infection also occurred after a pure culture had been 
accidentally drawn into the mouth. There are two other instances 
in which accidental infection occurred in man. 



ANIMAL PARASITES OF THE FECES. 

CLASSIFICATION. 

I. Protozoa. 

1. Rhizopoda Zoologists recognize six orders of this class of 

parasites, one of which is found in the human 
intestine and feces. 

2. Ameba (Entamoeba) The Entamoeba coli and E. histolytica (see page 

388). 

3. Flagellata s. mastigophora. . .Occasionally found in human feces (page 392). 

4. Cercomonas (Lamblia, Meg- 

astoma) Found in human feces (see page 394). 

5. Trichomonas hominis Found in human feces, less often in leukorrheal 

discharges, and in the urine (see pages 393, 484). 

6. Balantidium coli A parasite found in practically all parts of the 

Eastern Continent and in North America. Re- 
covered from the feces of man and those of the 
swine (see page 395). 

7. Trypanosoma A genus of protozoa found in the blood of man 

and in the cerebrospinal fluid of persons suffer- 
ing from sleeping-sickness. It is common in 
pus from abscesses of horses and in the blood of 
rats (see page 151). 

8. Protozoon of Laveran (mala- 

rial parasite) See Malaria (page 157). 

9. Piroplasma hominis A protozoon found in the blood of persons suf- 

fering from Rocky Mountain spotted fever (tick 
fever) (see page 155). 



384 THE FECES. 

II. Entozoa. 

1. Agamodistomum ophthalmo- 

bium (Fasciola ophthal- 

mobium) A rare parasite which invades the capsule of the 

crystalHne lens. Probably identical with the 

liver fluke. 

2. Ankylostoma (Uncinaria) 

duodenale and Americana. Infests the duodenum and small intestine; its 
ova are recovered from the feces (page 415). 

3. Anguillula aceti A parasite of the human urine (page 298). 

4. Ascaris canis (or mystax) 
. • 1 1 • -J (A genus of nematoid intestinal worms (page 

Ascaris lumbricoides r ■ • \ \ ^^. • j ^ ^ j • ^u r 



<. Ascaris lumoricoiaes r ■• \ X ^^u • ^ ^. ^ j ■ .1, r 

^ , (414); their ova are detected m the leces. 

6. Ascaris maritima J 

7. Cysticercus cellulosse (cysti- 

cercus of Taenia soHum) . . .Genus of family of hydatids, and distinguished 
by the caudal vesicle in which the depressed 
body of the animal rests. Found in muscles, 
meninges, ventricles, and brain. 

8. Cysticercus (C. tenuicollis) of 

Taenia marginata A rare intestinal parasite. 

9. Dibothriocephalus latus The fish tape-worm, which is commonly referred 

to as Bothriocephalus latus (page 402). 

10. Dicrocoelium lanceatum A variety of liver fluke (page 412). 

11. Diplogonoporus grandis .A rare parasite of the human intestine in 

Europe and North America. 

12. Diplosoma crenatus An entozoon four to eight inches long, which is 

bent upon itself at an acute angle. Habitat, the 
urinary bladder. May be passed with the urine. 

13. Dipylidium (Taenia) caninum. Dog tape-worm, rarely found in the intestine of 

man (page 407). 

14. Dracunculus medinensis Guinea-worm or thread- worm. Invades the 

areolar tissue and skin of the legs and feet (page 
149). 

15. Echinococcus polymorphus 

(hydatid of Taenia echino- 
coccus) Liver, spleen, lung, brain, meninges, and omen- 
tum. Larval form of the dog tape-worm, and 
develops in man as a hvdatid cvst (see also No. 
8). 

16. Eimeria bigemina Invades the intestinal epithelium of man and of 

animals (dog and sheep). 

17. Eustrongylus gigas The largest of this genus. Found in the human 

kidney and intestine; also in the kidney of the 
lower animals. 

18. Fasciolopsis buskii A trematode worm found in the gall-bladder 

and duodenum of residents of Asia. 

19. Fasciola haematobium Same as No. 34. 

20. Fasciola hepatica The common liver fluke (page 411). 

21. Fasciola hepatica ^gyptiaca .The Egyptian liver fluke (page 412). 

22. Fasciola hepatica angusta The narrow liver fluke (page 412). 

23. Filaria medinensis See No. 14. 

24. Filaria oculi or lentis May invade the eye, but it is also allied to 

Filaria perstans (page 147). 

25. Filaria sanguinis hominis Infests blood of man, animals, and birds. Spe- 

cies of filaria are common in crows, blackbirds, 
wild ducks, and the porcupine (page 147). 



ANIMAL PARASITES OF THE FECES. 385 

26. Heterophyes heterophyes Inhabits the small intestine. 

27. Monostoma lentis See No. 20. 

28. CEstrus hominis A bot-fly which deposits its ova in the skin; also 

in the external auditory canal (page 470). 

29. Opisthorcis noverca | r Trematode worms found in the gall-bladder 

30. Opisthorcis sinensis j \ and duodenum of residents of Asia. 

31. Oxyuris vermicularis A nematoid worm — pin-worm, seat-worm^-in- 

festing the rectum and vagina (page 414). 

32. Paragonimus Westermanii ...A parasite of the lungs, Hver, and connective 

tissue (page 435). 
^^. Pentastoma constricta , 

(Porocephalus con- ) f -^ genus of entozoa parasitic to man and ani- 
strictus) . • ( J ^^^- ""^ loi^g' cyHndric, annulated worm in- 

34. Pentastoma denticulatum j ll^^'!!^ ^^^ intestine;_ it may become encysted in 

(Linguatula rhinaria) . / ^ ^^^ ^^^^^ ^^^ ^^^^^ tissues. 

35. Schistosoma (Bilharzia) haema- 

tobium A genus of trematoid worms that inhabit the 

portal, bladder, hemorrhoidal, and pulmonary 
veins; its ova are to be found in the urine, feces, 
and sputum (pages 295, 436). 

35 A. Schistosoma Cattoi Resembles 35 except the ova escape into bowel 

and the worm invades arteries instead of veins. 

36. Strongyloides stercoralis (in- 

testinalis Cause of Cochin-China diarrhea (page 419). 

37. Strongylus bronchialis A nematode worm from the human bronchus. 

38. Strongylus gigas (Ascaris re- 

nahs) See No. 16. 

39. Strongylus subtilis Japanese diarrhea worm (page 421). 

Taenia acanthotrias A rare finding in man. 

40. Taenia africana See page 409. 

41. Taenia echinococcus See No. 15; also page 404. 

42. Taenia elliptica See same as 13. 

43. Taenia flavopunctata (Hy- 

menolepis diminuta) A parasite rarely found in the intestine of man; 

its ova closely resemble the ova of Taenia solium. 

44. Tsnia (Davainea) madagas- 

cariensis See page 409. 

45. Taenia marginata The dog and sheep tape- worm (page 406). 

46. Taenia mediocanellata The beef tape-worm (page 399). 

47. Taenia (Hymenolepis) nana.. Dwarf tape-worm which invades the intestine 

of man and the lower animals (page 406). 

48. Taenia solium Pork tape-worm. A rare American parasite 

v/hich inhabits the small intestine of man (page 
398); also No. 7. 

49. Trichinella (Trichina) spiralis The adult worm invades the intestine of man 

and of the lower animals, and is taken into the 
stomach through infected pork. The larval 
form of the worm is deposited in the intestinal 
wall, and from there migrates to all parts of the 
body. These larva become encysted in the 
muscles (page 422). 

50. Trichocephalus dispar (Tri- 

churis trichuria) Found in the cecum and colon of man, and is 

associated with the ankylostoma. The ova are 
detected in the feces (page 418). 
25 



386 



THE FECES. 



III. ECTOZOA. 

1, Acarus (Demodex) follicu- 

lorum Invades the sebaceous follicles of the skin, and 

also the conjunctiva. 

2. Pulex (Sarcopsylla) penetrans 



(chigo) 



.A variety of tick found in Brazil and tropic dis- 
tricts. It invades the skin and cellular tissues. 



GROSS EXAMINATION. 

Of the various methods employed for the diagnosis of intes- 
tinal parasites, a microscopic study of the feces is most reliable. 
There are other methods of study, however, which should not be 
neglected. It is possible, at least, to suspect the presence of 
intestinal parasites from an examination of the blood, since 
eosinophiha is often associated with such infections. 

A gross examination of the feces is of equal importance in the 

adult and in the child; in 
some cases such an examina- 
tion may reveal segments of 
a tape- worm (Fig. 151); in 
the case of nematode infec- 
tion the adult worm may be 
seen. Adult round-worms 
are likely to appear in the 
feces after the administra- 
tion of anthelmintics, and 
are at times found after the 
patient has taken a liberal 
dose of calomel. During the 
first stage of trichinosis, when 
there is an associated diar- 
rhea, the adult trichinella may 
be found in the feces (Fig. 173). The uncinaria and the oxyuris 
may also be detected in the diarrheal discharges. The technic 
for the detection of these parasites differs in no way from that 
outlined for the detection of the head of the tape- worm (page 397). 
When there is severe hook-worm infection, the color of the 
stools is often reddish brown. Ashford states that this color is 
probably due to the presence of blood in the stools, and that the 
blood reaches the intestinal canal from the openings made in the 
intestinal wall by the biting of the parasites. He further suggests 
that the anemia produced by such an infection is in part due to the 
continuous oozing of blood from the intestinal mucosa. 




Fig. 144.— Magnifier mounted on tripod, for 
gross examination of feces for parasites. 



GROSS EXAMINATION. 387 

Blotting-paper Test. — Place several ounces of the fresh stool 
on a white liher-paper, wrap the paper tightly around the feces, 
and allow it to stand for several hours ; then unwrap the package 
and examine the paper. In severe and sometimes in mild cases 
of hook-worm infection a distinct reddish-brown stain is present. 
This test is reliable in 70 per cent, of cases (Stiles). 

Microscopic Study. — The microscopic characteristics of the 
feces have been discussed in connection with each intestinal para- 
site, but in a general way it may be well to consider a few points 
of practical interest. In collecting feces for microscopic study 
I to 5 gm. of the stool may either be wrapped in a piece of paper 
or placed in a wide-mouthed bottle and sent to the laboratory. 
It is better to prevent the stool from drying until the examination 
is completed, because while an expert microscopist may examine 
a stool that is several days old, far more satisfactory results are 
to be obtained from the study of fresh specimens. 

Washing of the Feces. — Take one or more ounces of either 
the fresh or the dried feces, add one to two quarts of water, and 
stir until the feces are well mixed; allow to stand for a time to 
permit of sedimentation. Pour off the floating matter and the 
water down to near the sediment; repeat this washing several 
times and until no material floats upon the surface after sedimen- 
tation. Place the washed sediment in a conic glass and allow it 
to stand for a few hours, when it will be found to contain ova 
of whatever parasites may be present in the intestinal canal. 
Washing of the feces is not necessary for the detection of the 
Amoeba. 

Apparatus. — The apparatus necessary for microscopic exam- 
ination of the feces includes a microscope, glass slides (two by 
three inches), large square cover-glasses, and a platinum needle, 
or, what is more commonly employed, a match-stick (see Detection 
oj Ova of the Uncinaria, page 417). At least ten shdes should be 
examined before a negative diagnosis is given. 

Cautions. — It is of utmost importance that the feces be 
kept in a bottle that is well corked in order that the specimen be 
protected from flies. The greatest care should be exercised to 
prevent soiling of the hands during the examination, and all 
glassware should be placed in boihng water after use. It is well 
for the operator to remember that the feces of persons infected 
with tape-worm are highly dangerous to man. 

A microscopic study of the feces is of no value unless one is 
familiar with the appearances of the eggs and embryos of the 
different animal parasites (see Plates 26, 27). All suspected 
objects should be studied most carefully, since plant-cells and 



388 THE FECES. 

fibers which closely resemble both the ova and the embryos of 
intestinal worms are always present in the feces. 

The ova of animal parasites may appear in the feces when the 
adult parasite resides elsewhere than in the intestinal canal. 
The ordinary hver-fluke (page 411); the paragonimus (page 435), 
which invade the lungs, and the Schistosoma haematobium, which 
invades the vesical veins (page 295), are examples. It is, therefore, 
necessary that the sputum and the urine be studied conjointly 
with the feces in the diagnosis of animal parasites. 

INTESTINAL COCCIDIOSIS, 

It has long been known that coccidia were Hable to infest the 
intestinal wall of domestic animals. Stiles has recently reported 
an interesting example of intestinal coccidiosis occurring in the 
sheep.* The Coccidium bigeminum (Eimeria bigemina) will be 
found to vary in length from 0.008 to 0.015 ^^- According to 
Stiles, the size of this parasite varies, depending upon the animal 
(host) in which it has developed. Intestinal coccidiosis may 
develop in man. The accompanying illustrations (Plate 24) will 
serve to explain the peculiar features of this parasite, as well as 
to describe the sHght differences between the Coccidium bigeminum 
and other coccidia. 

RHIZOPODA. 

The feature characteristic of this class of organisms is that 
its movements are caused by the throwing-out of prolongations, 
or pseudopods, from its body. These pseudopods result from 
protoplasmic activity, which enables the cell to protrude a pseudo- 
pod from any portion of its body. Rhizopoda are occasionally 
met with in the human feces. 

Amoeba Coli. — The member of the above group of animal 
parasites which concerns us most as cHnicians is the Amoeba coli 
(Losch), which was first described in 1875. Losch, at this date, 
detected for the first time the Amoeba coli in the feces of persons 
suffering from tropic dysentery. At present the Amoeba coli has 
been found in the feces of dysenteric patients in practically all 
parts of the civilized world. Amebic dysentery has received special 
study in India, China, Japan, and in European and American 
tropic districts. 

Cases have been transported from the tropics to all portions 
of the world, yet the disease seldom, if ever, develops in temperate 
climates. 

I have studied both sputum and feces in which amebae were 

* "Jour. Comp. Med." and "Vet. Arch.," vol. xiii No. 5, pp. 319, 325. 



PLATE 24. 




1-^ I 



7- 




L ; -.v^F- 



7- 



7^- 



//- 



?{.?%. 






/^r- 



Z^- 



^- 



r- 



^ 






/^-- /7- 7"^- // 



/ - 




j?<i' 



1-7. Sporozoa (probably Coccidium perforans) from the intestinal epithelium 
of a sheep: i, Epithelial cell containing single parasite; 2, free parasite; 3, the 
plasma has receded from cyst-wall; 5-7, two to four parasites in each cell (Stiles). 

8. Portions of a villus of dog's intestine, showing eleven Coccidia bigemini. 

9-14. Various stages in the development of Coccidium bigeminum (highly 
magnified) (Stiles). 

15-20. Coccidium oviforme of rabbit (Stiles, from Balbiani): 15 corresponds 
to 3; 16, plasma divided into two sporoblasts; 17, further division; . iS, sporo- 
blasts are elongated; 19, they have become spores. 

21. Coccidium bigeminum to show four sporoblasts and rest of segmentation 
(Stiles). 



EHIZOPODA. 



389 



present (Fig. 145). The patients from whom the specimens were 
obtained had previously resided in the Phihppine Islands. Cun- 
ningham has found that the ameba is fairly common in the stools of 
cholera patients. Grassi and Massiotin report having found amebae 
in normal feces. George Dock, of Ann Arbor, has also detected 
amebae, indistinguishable from the Amoeba coli, in normal feces. 

The fact that amebae have been found in normal feces and 
in feces of diseases other than dysentery has led to the sup- 
position that there are two species of Amoeba — the Amceba 
{Entamoeba) coli, which is harmless, and the Amoeba (Entamoeba) 
histolytica, which is concerned in the etiology of tropical dysentery, 




Fig. 145. — Amoeba coli and cluster of epithelial cells from the sputum ; private patient 
(obj. B. and L. one-twelfth oil-immersion). 



and of tropical abscess of the liver and lungs. A case of the 
latter condition has been studied by the author.* 

Collection of the Feces. — In the study of feces for the de- 
tection of the Amoebae the precautions already described on 
page 356 should be taken in the collection of the specimen. 

The rectal mucus is most likely to contain the amebae, and is 
best collected by introducing a large rubber catheter into the 
rectum. It is my practice to cut several rather roughly outlined 
openings in the side of the catheter. Immerse such a catheter 
in warm water, and introduce it into the rectum for a distance of 
from three to six inches or more. The mucus, blood, or pus that 

* "Proc. Phila. Co. Med. Soc," Sept., 1902. 



390 THE FECES. 

may cling to the catheter is most Hkely to contain the amebae. 
This material is equally valuable in searching for the ova of prac- 
tically all intestinal parasites. The administration of a vermicide 
does not appear warrantable except after positive results are 
obtained from a study of the rectal mucus, blood, or pus. 

Detection of the Parasites. — Place a small drop of the 
Hquid portion of the feces or of the mucus, blood, or pus upon the 
center of a sHde, add a drop of distilled water, mix the specimen 
with the water, and allow a cover-glass to fall gently upon the 
mixture. Warm one end of the slide slightly and then examine 
the specimen with a one-sixth or a one-eighth objective. With the 
magnification thus obtained it is possible to detect the ameba, 
and then further study may be made by bringing individual organ- 
isms into the field of an oil-immersion objective. 

The Amoeba coli is a unicellular animal parasite which varies 
from 13 to 37 /i in diameter.* Whenever the feces or liquid con- 
taining the Amoeba coli is allowed to become cold, the amebae at 
once assume a more or less spheric form and show no evidence 
of movement. During this quiescent state they are found to vary 
greatly in size ; their surface is in part granular, while the remain- 
ing portion is hyaline, although the entire organism may display 
a more or less granular surface. It is impossible to detect the 
Amoeba coh in the feces when the dejecta is at room-temperature, 
but when the sHde containing the feces is placed upon a warm 
stage or heated gently over a flame and studied under a one- 
twelfth oil-immersion objective, the spheric granular bodies 
present in the cold specimen will be found to have assumed irreg- 
ular shapes. 

By watching an individual ameba it will be seen to throw out 
distinct prolongations (pseudopods) of its protoplasm. The pro- 
jected portion of the cells is at first a mere bulging of the cell- wall; 
it then becomes oval, and finally appears Hke a pedicle. The 
pseudopod does not contain any of the granular protoplasm. 
After the cell- wall has been protruded for some distance, a proto- 
plasmic current may be seen extending into this protrusion, and 
the granular protoplasm of the cell flows from its former resting- 
place to this protruded part of the cell. By the time all the gran- 
ules have completely changed their position the cell will, in all 
probability, have become more or less spheric in outline — an 
apparent retraction of the protruded portion of the cell-body. 

These movements are followed by a projection of the proto- 
plasm from another portion of the cell-body, when the granules 
again change their position. 

* Dock, "Daniels' Texas Med. Jour.," 1891. 



RHIZOPODA. 391 

Caution, — It is a very easy matter for the inexperienced to 
mistake epithelioid cells, which are often present in the feces, for 
the Amoeba coli. These epithelioid cells display a violent proto- 
plasmic motion, and there is a slight movement of the cell's margin, 
but true pseudopods are not formed. 

In all active amebae a variable number of hyaline areas 
are to be seen (vacuoles). These vacuoles, as a rule, number 
from two to four, and are highly conspicuous in the motile para- 
site. They may also be detected in the non-active amebae. The 
vacuoles may be situated within the granular portion of the para- 
site, and it is quite common to find the protoplasm more granular 
around the vacuoles than at other portions. At times, imme- 
diately surrounding the vacuole, there is a series of clear vesicles 
which are nearly uniform in size. These vesicles may occur at 
any portion of the body, and are more pronounced in some or- 
ganisms than in others. During the ameboid movements of the 
parasites both the vacuoles and the vesicles appear to change in 
size. 

Nucleus. — The nucleus of the Amoeba coli is fairly charac- 
teristic, although it is much less conspicuous than are the vacuoles. 
The nucleus is best seen when there is a low degree of illumina- 
tion; in fact, amebae are best studied with a small amount of 
light. The nucleus of the Amoeba coli will be found quite dis- 
tinct in certain parasites (Fig. 145), while in others it is detected 
only after the most careful microscopic study. 

I have endeavored, in the accompanying illustration (Fig. 145), 
to set forth the peculiarities known to the Amoeba coli. These 
features are in a great measure common to all amebae. 

Life-cycle. — The life-cycle of the Amoeba coli within the 
human body is a subject which has received much research, 
and until quite recently but little definite knowledge has been 
obtained. A knowledge of the methods through which other 
similar animal parasites develop has served to direct various 
investigators, among whom Grassi and Doflein and also Clarke * 
have considered the development of the Amoeba coli in compari- 
son with that of the malarial parasite. Schaudin proved that 
nuclear division is not constant and regular in the "Amoeba coli," 
but, instead of this, a fragmentation of the chromatin takes place, 
"the remnant of the nucleus being expelled from the parasite." 
This division of the chromatin is followed by the formation of 
small spheric bodies, each of which is thought to contain a portion 
of chromatin. Schaudin further showed that these spores were 
capable of producing intestinal symptoms and lesions. The above 

* "Protozoa and Disease," p. 36. 



392 THE FECES. 

peculiarities are not known to be common to other amebae found 
in the intestinal canal. More recently Surgeon Charles Craig * in a 
preliminary note, in addition to making reference to the study 
of 748 cases of amebic dysentery, has considered the development 
of the ameba. 

Blood-cells. — Individual amebae are at times seen which 
have engulfed one or more red blood-cells, leukocytes, bacteria, 
and granular detritus. The red cell is often situated near the 
center of the ameba, and may be completely surrounded; in fact, 
it is sometimes partially obscured by the granular protoplasm. 

Stain. — -The Amoeba coli stains with the ordinary anilin 
dyes (a 2 per cent, aqueous solution of methylene-blue) and 
carbolfuchsin. It is with some difficulty that the ameba is well 
stained when in the feces; but the parasite is readily stained when 
in the sputum or in pus from amebic abscesses. When stained 
with methylene-blue and fuchsin, full-grown amebas display from 
one to three vacuoles which are unstained. There are also to be 
seen numerous small, round or oval, dimly stained areas which 
are rather regularly disseminated throughout the protoplasm. 

Clinical Significance. — Amoebae coli may be found in 
the stools during the course of amebic dysentery. They are often 
present in the fluid obtained from the so-called amebic abscess of 
the liver, and from the sputum in cases where hepatic abscess 
has ruptured into the lung (see Sputum^ page 436). 

FLAGELLATA. 

Members of the group flagellata or mastigophora are char- 
acterized by the fact that each organism displays from one to 
eight flagella. These flagella, by their active movements, render 
the animal capable of locomotion. It is not uncommon to find 
members of this class of parasites in the feces. 

Cercomonadina. — The parasites of this family are small, 
and may be either oval or shghtly elongated in outhne. They are 
provided with one rather long flagellum at their anterior extremity, 
and contain one or more vacuoles. These parasites are also capa- 
ble of ameboid movement, and may be seen to protrude pseudo- 
pods from their posterior extremity. The cercomonas described 
by Davaine and Lambl is a representative of this family of para- 
sites (page 394). 

Tetramitina. — Another parasite, the tetramitina, is a small, 
elongated body which possesses an undulating membrane and four 
distinct flagella. This parasite tapers gradually at one extremity 

* "Amer. Med.," Feb. 20, 1904. 



FLAGELLATA. 



393 



and has a distinct nucleus. Tetramitina may be detected in the 
feces, in the vaginal discharges, and in the urine. They are 
probably identical with the trichomonas and cercomonas seen in 
these situations (Fig. 146). 

Trichomonas. — This parasite has received a variety of names, 
many of which refer to the situation from which it was recovered, 
while others refer to its pecuHar biologic characteristics. The 
Trichomonas intestinalis is an animal parasite (Fig. 146) which 
may be oval or spindle-shaped, and which varies in size from 
0.012 to 0.03 mm. by o.oi to 0.015 mm. 

The trichomonas is provided with an undulating membrane 




Fig. 146. — I, 2, 3, 4, 5, 10, and ii, Various forms of Cercomonas intestinalis (after Leuck- 
art and Lambl). 6, 7, 8, and 9, Various forms of trichomonas {after Scanzoni and Kolliker 
and Dock). 12, Encysted form, and 13, adult form, of Megastoma entericum (Cercomonas) 
(after Grassi and Schewiakofi). 



which extends from the parasite as a tail-Hke projection. Four 
flagella of varying sizes project from the anterior pole of the or- 
ganism. It is very difficult to detect either the undulating mem- 
brane or the flagella when the animal is in motion. When a given 
liquid is known to contain the trichomonas, it is w^ll to add a 
solution of mercuric chlorid (1-6000) to it. After this treatment 
both the flagella and the nucleus of the parasite become slightly 
more conspicuous. Specimens thus treated will be found to 
stain with the ordinary anihn dyes, and under these conditions the 
nucleus may be clearly outlined. The trichomonas is said to 
possess the faculty of ameboid movements. 



394 THE FECES. 

In the study of Philadelphia water I found that by the addition 
of a small amount of hay, for the purpose of developing certain 
bacteria, many small organisms which were apparently identical 
with the trichomonas were invariably found after the hay and 
water had been allowed to stand at room-temperature for a few 
days. ■ 

The technic necessary for the detection of the trichomonas 
is essentially the same as has been described for the detection of 
the Amoeba coh (page 390). 

Cercomonas intestinalis (Lamblia duodenalis) . — Grassi has 
described this parasite under the name of Megastoma entericum 
(Fig. 146). Davaine refers to this parasite as the Cercomonas 
hominis, and many other writers have given this organism names 
more or less expressive of the location in which it has been found, 
or of its characteristic pecuharity. It does not appear practical 
to me to endeavor in this volume to set forth the distinctive 
differences known to exist between species of the cercomonas ob- 
tained from the various sources. 

Generally speaking, the cercomonas is pear-shaped, and 
varies in length from o.oi to 0.21 mm. In breadth the cercomo- 
nas varies between 0.0075 ^.nd 0.05 mm. The longer forms of 
this parasite are sometimes more or less S shaped. At the 
anterior portion of the cercomonas there is a fairly well- 
defined indentation, which is the peristome or mouth of the 
animal. The cercomonas, as a rule, has eight flagella, which 
project from the body in pairs. It is impossible to see these 
flagella in the actively motile parasite, but they are readily seen 
after treatment with a 1-5000 solution of mercuric chlorid. 
It is to be noticed that the flagella of the cercomonas are directed 
backward (Fig. 146). The first pair are given off from the sides 
of the anterior opening of the parasite, and two additional pairs 
of flagella are given off just posterior to this depression. The 
fourth pair of flagella project from the tail. It is often very 
diflicult, even in the well-prepared specimen, to detect the eight 
flagella and, in fact, it is the rule to find many of these flagella 
twisted or plaited together to form a rather large flagellum. 

This organism, when in its quiescent state, may assume an 
oval, elliptic, or spheric shape, and its flagella may not be ap- 
parent. For this reason and for many others my experience has 
indicated that it is not at all times possible to distinguish the cer- 
comonas from other similar animal parasites. 

Clinical Significance. — The cercomonas may be found in 
the feces of man and the lower animals. It is rarely encountered 
in the vaginal secretions and in the urine. Its pathogenic power 
is questioned. 



FLAGELLATA. 



395 



Balantidium Coli. — The Balantidium coli (Paramoecium coli) 
is an oval organism which measures about i mm. in its greatest 
diameter (Figs. 147, 148). This organism dijEfers from the 
organisms just described in that its entire body is covered v^ith 
fine ciKa. These ciHa are thickest surrounding the mouth of 
the parasite, and are thinly distributed over the body and around 
the anus. The Balantidium coli has a pale nucleus and from 
tv^^o to four vesicles. 

Within the body of the parasite small particles of starch may 
be seen, and at times droplets of fat are detected. 

Clinical Significance. — Infection with the Balantidium coli 
is supposed to take place from the dejecta of swine. This 
parasite has been known to affect man in various portions of 
Europe, Asia, and North America. Ehrenroth,* in addition to 
reporting a fatal case of dysentery due to infection with the Balan- 
tidium coH, describes interesting pathologic changes present in 
the stomach and intestine (ulcerations). All together 89 cases of 





Fig. 147.— Balantidium coli (after 
Malmsteii). 



Fig. 148.— Balantidium (Paramoecium) 
coli (Eichhorst). 



persistent diarrhea due to this parasite have been reported. It 
is of special interest to note that the profound anemia caused by 
the Balantidium coli resembles closely that present in the later 
stages of gastric carcinoma. 

The Balantidium coH has been found in the feces of persons 
suffering from infection with the Dibothriocephalus latus; and it 
has been suggested that other intestinal parasites render the gastro- 
intestinal canal in a receptive state for infection with the Balan- 
tidium coli. In the fatal cases ulcerative coKtis appears to be 
regarded as the cause of death. 

Detection. — The technic necessary to detect the Balantid- 

* " Zeit. f. klin. Med.," vol. xlix, p. 251. 



396 THE FECES. 

ium coli in the feces differs in no way from that described for the 
detection of the Amoeba. 



TAPE-WORMS (CESTODES), 

The habitat of this variety of parasites is the small intestine, 
where they give rise to considerable irritation, which results in a 
variable amount of intestinal catarrh. As the result of the intes- 
tinal catarrh, body depletion, toxemia, decided nervous manifes- 
tations, and severe anemia may follow infection with such parasites. 

In reference to tape-worms in general it may be said that the 
head of the parasite is extremely small, and in some of the species 
resembles the head of a black pin. The head of the tape-worm 
may be armed with a complete crown of hooklets, and may also 
possess deeply pigmented or colorless depressions, which serve as 
sucking cups (Figs. 150, 158). The segments (proglottides) of 
the tape- worm always vary greatly in size (Fig. 151) — the longer 
the tape- worm, that is, the farther from the head, the larger is the 
segment. Extending from the largest of the segments toward the 
head, it is immediately apparent that each segment lessens in 
size until the neighborhood of the head of the parasite is reached, 
where the segments appear to the naked eye as a slightly flat- 
tened thread. The segments of the tape-worm are of a yellow- 
ish-white or bluish- white color. 

The technic for the recognition of animal parasites in the human 
feces is of special importance in view of the fact' that there is no 
other secretion or excretion wherein the offending object is sur- 
rounded by so large an amount of debris. It is fairly easy, how- 
ever, to detect segments of tape- worms and the adult forms of other 
parasites when present in the feces. The search for the head of 
a tape- worm in the feces, after the administration of vermicidal 
drugs, is of paramount importance in the study of the parasite. 

Removal of Tape-worms. — Before attempting to remove a 
tape-worm from the intestinal canal the physician should be sure 
that the patient's stomach is entirely empty, and that since his 
last meal sufficient magnesium citrate solution has been adminis- 
tered to produce two or more copious bowel movements, so that 
the greater part of the intestinal mucus has been expelled. It 
is the habit of the tape- worm to bury its head in the folds of the 
intestinal mucous membrane (valvulae conniventes), and mucus 
collects about the point at which the worm is anchored to the in- 
testinal wall. Unless this fortification of mucus be removed before 
the administration of a vermicide, it is improbable that the drug 
can reach the head of the parasite. 



TAPE- WORMS. 397 

To Detect the Head. — The majority of failures in the treat- 
ment of tape- worms is due to the inabihty of the host to expel the 
head of the parasite, and since this is most important, I recom- 
mend the following routine procedure for the accomplishment of 
the object: (i) Empty the bowels by means of sahnes, so that no 
undigested food remains in the alimentary tract, and to insure 
that the head of the worm is uncovered by the removal of all 
intestinal mucus. (2) Administer a vermicide. (3) Follow in 
from four to six hours by another saHne. (4) When the worm 
begins to escape from the anus, direct the patient to take a com- 
fortable seat, so that the parasite may be received in a clean 
vessel containing water. (5) It is all-important that the patient 
should sit on one commode from the time he observes that 
the worm is diminishing in size until the entire parasite is 
passed {the nearer the head, the smaller are the segments). When 
wdthin a few inches — ten to twelve — of the head, the worm appears 
as a pale, sUghtly flattened thread, and its segments are not dis- 
tinct. (6) The head is the last portion of the worm to be passed. 
While any part of the parasite is 
protruding from the rectum the 
probabihties are that the head 
has not yet escaped. 

Given a specimen collected 
in this manner, add a quantity 
of water and stir gently with a ^ig. i49.-Dish for study of feces. 

glass rod, so that the worm will 

fall to the bottom of the vessel. Decant one-half or more of the 
liquid, and replace it with clean water; repeat this washing until 
the worm is cleansed. Transfer the worm with some of the water 
to a clear glass dish 10 by 12 by 3 inches (Fig. 149), and place the 
dish on a white surface (towel). Remove all the large segments 
of the parasite by a glass rod, drawing them over the edge of the 
first dish and allowing them to fall into a second dish containing 
water, taking care not to break the parasite. 

After all large segments are removed the head may, as a rule, 
be readily detected by the naked eye floating among the remaining 
thread-Hke portions of the parasite. In searching for certain 
smaU parasites a hand-glass is found of service. The head 
should be transferred to a 10 per cent, glycerin solution and 
preserved for further study. In mounting the head of a para- 
site a sHde provided with a concavity of sufficient depth to accom- 
modate its thickest portion is most satisfactory. The specimen 
may be preserved by mounting it in cast medium, Farrant's 
medium, glycerin, or glycerin-jelly. 




398 



THE FECES. 



Taenia Solium. — This parasite, the pork tape-worm, is fairly 
common in Europe, Asia, and Africa, but it is rarely found in 
America; and whenever found in this country, the question of the 
patient's having been abroad should be thoroughly investigated. 
The Taenia solium when in the human intestine may vary greatly 
in length, but this is of minor importance, since the length of any 
tape-worm does not appear to influence materially the symptoms 




Fig-. 150. — Taenia solium: i, Head (obj. B. and L. two-thirds); 2, segments; 3, head 
and neck (natural size) ; a, ova (obj. B. and L. one-sixth). 4, Head of Dibothriocephalus 
latus (magnified). 5, Dibothriocephalus latus (natural size) ; b, ova (magnified). 



resulting from infection with such a parasite (see Method for 
Finding Head, page 397). 

The head of the Taenia soHum (Fig. 150) is provided with four 
pigmented sucking-cups, which are best seen when examined with 
a two-thirds objective. It is usually possible to outhne clearly a 
complete crown of booklets at the tip of the head with a one-fourth 
objective. The fully matured proglottides (segments) are about 
10 mm. long by 3 to 5 mm. wide (Fig. 151). The matured pro- 
glottides of the pork tape-worm present certain features which 



PLATE 25. 



^'^^\ 



2- 







11 K 



T. 



r\' 



1. Cluster of cysts (Cysticercus cellulose) recovered from lateral ventricle of 
brain in Lloyd's case (original). 

2. Cyst found in fourth ventricle (original). 

3. A piece of pork infested with pork-measles (Cysticercus cellulosae) (Stiles). 

4. Isolated pork-measle bladder-Avorm (Cysticercus cellulosae), with extended 
head, greatly enlarged (Stiles). 

5. Young cysticerci (Cysticercus tenuicollis) of the Taenia marginata (Curtice). 

6. Cysticercus tenuicollis with head extended from body, from a steer (Stiles). 



TAPE-WORMS. 



399 



serve to distinguish them 
from those of the beef 
tape- worm, so that by a 
study of these segments a 
diagnosis of the species 
present in the intestine 
may be made. Segments 
of the Taenia soHum have 
a longitudinal canal or 
uterus from which several 
branches (eight to four- 
teen) extend laterally. 

The ova of the Taenia 
solium are secreted con- 
stantly, and appear in the 
feces in large numbers. 
They are round and, when 
fully developed, are fur- 
nished with a shell upon 
which it is possible, by 
carefully focusing the mi- 
croscope (one-sixth objec- 
tive), to distinguish fine 
radiating lines. Firm 
pressure upon the cover- 
glass usually results in 
rupturing the operculum 
(shell), which often flies 
into many pieces. 

When ova of the Taenia 
solium enter the human 
stomach from the mouth 
or are regurgitated from 
the intestine, the parasite 
develops only to its larval 
stage. Each larva subse- 
quently becomes encysted 
in the human tissues or 
viscera, where it is known 
as the Cysticercus cellu- 
losae (Plate 25). 

Taenia Mediocanel- 
lata. — The beef tape- 
worm (Taenia saginata) is 
found in nearly all parts ffir'^rS-Js? "'"'" ^"^^"'^^ - ^'^^^ ^^''^' 




Fig. 151. — Several portions of adult pork-measle 

S. 



ion of Animal Industries, U 
Dept. of Agriculture). 



4oo 



THE FECES. 



of the civilized world, and is especially common in North America. 
The length of this parasite may at times be practically incredible. 
In my own experience I have seen a parasite 36 J feet long, which 
was obtained from an inmate of the Philadelphia Hospital. There 
are many records of cases in which much longer specimens of the 
Taenia saginata have been recovered from man. 

Head. — The head of the beef tape- worm (Fig. 152) is of a 
dark-blue color and is said to be much larger than is the head of 
the Taenia solium. It is best studied under a low-power objec- 
tive (two-thirds). It has four depressed sucking-cups, but, in 




[52. — Taenia mediocanellata : i, Largfe and small segments (natural size); 2, head (obj. 
B. and L. two-thirds); 3, o\a (obj. B. and L. one-sixthj; 4, neck. 



Striking contrast to the head of the Taenia solium, it has no hook- 
lets; a tapering neck displays a faintly granular surface; slight 
transverse striations extend from the pigmented portion of the 
head (Fig. 152). 

Proglottides. — The mature proglottides of the beef tape- 
worm are much broader and thicker than are those of Taenia 
solium. Segments may escape from the rectum at any time, 
because they possess a limited power of independent movement. 
I have placed fresh mature segments of the beef tape- worm .and 
of the dog tape-worm (Taenia marginata) under a two-thirds 



objective and watched 
their movements care- 
fully. While such a 
study is most interest- 
ing, it can scarcely be 
recommended as prac- 
tical. The individual 
segment of the beef 
tape- worm has a central 
canal (uterus) from 
each side of which 
a great number of 
dichotomously dividing 
branches are given off 
(Fig. 153). This is the 
distinguishing feature 
between the proglot- 
tides of the beef tape- 
worm and of the pork 
tape-worm. 

Ova. — The ova of 
the Taenia mediocanel- 
lata (Fig. 154) resemble 
those of the Taenia sol- 
ium closely. The slight 
difference in size is not 
sufficient for diagnosis 
unless one resorts to 
measurements. These 
ova also escape with 
the feces. 

The ova of the tape- 
worm are best studied 
by placing a ripe seg- 
ment upon a shde and 
tearing a small piece 
from its center. Place 
this piece upon a second 
slide, and apply gentle 
pressure or tease with 
a needle to liberate the 
ova. Discard the tissue 



Fig- 153- — Portions of adult 
beef-measle tape-worm (Taenia 
saginata or Taenia mediocanel- 
lata) from man, showing head 
and gradual increase in size of 
segments; natural size (Stiles, 
Bullet. 15, Bureau of Animal 
Industries, U. S. Dept. of Agri- 
culture). 

26 




401 



Fig- 153- 



402 



THE FECES. 



of the segment, add a drop of water to the liberated ova, and 
apply a cover-glass (Fig. 154). Specimen smears of the ova of 
the tape-worm prepared in this manner and fixed by heat (see 
Blood, page 74) stain well with anilin dyes. I have obtained 

most satisfactory results by staining 
such specimens for ten minutes with 
Delafield's hematoxylin. 

Dibothriocephalus Latus. — 
The Dibothriocephalus latus (Taenia 
lata of Linne) or fish tape-worm is 
a form of worm common in all 
countries bordering upon the Bal- 
tic Sea; it is also common in the 
vicinity of Lake Geneva and in 
Holland. This parasite, as a rule, 
appears to infect persons living in 
damp and marshy districts. Mul- 
tiple infection may occur, as has 
been shown by my esteemed friend 
and teacher, the late Dr. Frederic A. Packard, who reported such 
a case from the Pennsylvania Hospital. Dr. Robert N. Willson* 
reports the case of a female infected with at least two bothrio- 
cephali. Willson is of the opinion that there were three parasites 
present, but he was able to find only two heads of the Dibothrio- 




Fig. 154.— Taenia mediocanellata. 
Ova from the segment (obj. Spencer 
one-sixth). 






Fig. 155. — Dibothriocephalus latus (fish tape-worm) : A and B, Twin segments (R. N. 

Willson). 



cephalus latus. The accompanying illustration (Fig. 155) from 
Bremser was modified by Willson to represent the parasites re- 
covered by him and to show twin segments, A and B. 

The parasite varies greatly in length, the observations of many 

* "Amer. Jour. Med. Sci.," Aug., 1902. 



TAPE-WORMS. 403 

writers having established from 2 to 5 meters (6 to 30 feet) as 
the extremes. 

Head. — The head of the Dibothriocephahis latus is 2 or 3 mm. 
long by about i mm. broad. It is perfectly ovoid (Fig. 150, 4 and 
5) in contour, and closely resembles the expanded portion and 
handle of a spoon. Detection of the head of the dibothriocephalus 
in the feces is accomplished in the manner described on page 397. 

To the naked eye the head of this worm corresponds in size to 
that of a small pin. It may be of hght-gray or pearl-white color; 
it is sometimes colorless. In striking contrast to both the beef 
and the pork tape-worm the dibothriocephalus (fish tape-worm) 
possesses neither booklets nor suckers. The booklets, which 
were present in the early stages of development, are lost before the 
parasite is matured. There is a narrow groove on each side of the 
head, which possibly serves for attachment of the parasite to the 
intestinal wall. ' ' Cutaneous glands are to be found in the head, 
but are absent in the body." Muscle-fibers and two distinct 
nerve-cords have also been noted, the latter apearing like two 
roundish or kidney-shaped spots of granular appearance which 
gradually approach one another toward the anterior portion of the 
head and are finally united in a loop by a transverse connection 
(Leuckart). There is no distinct neck interposed between the 
head and the small (first) segments. 

Proglottides. — The mature proglottides do not escape from 
the rectum singly, as is observed in the case of the beef tape-worm; 
but these segments are, as a rule, passed in large numbers — one 
foot or more of the parasite passing at a time. The individual 
segment is very thin at a point near the head, as is shown 
by the accompanying illustration. They gradually increase in 
size, the largest segments being those farthest from the head. 
The small segments appear to be greater in length than in breadth, 
the medium-sized segments being nearly square. The mature 
segment varies from 2.5 to 4.5 mm. in length, and from 4 to 14 mm. 
in width. 

At the center of each segment there is a dark or slightly bluish 
spot, indicating the position of the ovary. When studied under 
a low-power objective (two-thirds), this area appears as an imper- 
fect roset. According to Willson, these rosets deepen in color 
in proportion to the number of ova contained. In segments 
from which many or all of the ova have been discharged the 
rosets are light in color. Rosets and ripe ova are found in the 
segments, about 500 mm. (19.5 in.) distant from the head. 

Ova. — Fully matured segments show the body of the uterus 
to be so packed with ova that the center of the segment protrudes 
slightly. 



404 



THE FECES. 



When there exists infection with Dibothnocephalus latus, the 
feces will be found to contain the ova of this parasite; and when 
detected in the stool of man, they are of great diagnostic value. 
These ova are elliptic or ovoid in contour, and, as a rule, of a 
muddy-white, brownish-white, or brown color. The ova of the 
dibothriocephalus vary from 0.06 to 0.07 mm. in length, while 
the width of the ovum is usually equivalent to about one-half that 
of its length. At one end of the ovum it is possible to discern, by 
the aid of a one-sixth or one-eighth lens, a faint 
hyaline band which outlines an apparent lid (Plate 
27). This lid may be either closed or partially 
opened. In this connection it may be well to 
refer the reader to a diagram of the ova of the 
Trichocephalus dispar (Plate 26). Upon two 
occasions I have been asked to examine feces 
wherein a diagnosis of infection with the bothrio- 
cephalus had been made, and in both cases I 
found ova of the trichocephalus present only. 

Taenia Echinococcus. — The Taenia echino- 
coccus, or small dog tape- worm, does not infest 
the intestine of man, but is commonly to be 
found in the dog, wolf, and fox. On account 
of the fact that the larval stage (Echinococcus 
polymorphus) of this parasite often develops 
in man, causing the so-called hydatid cyst, it 
may be of value to present the accompanying 
illustration (Fig. 156) of the adult worm. 

Characteristics. — The Taenia echinococcus is 
about one-fourth of an inch in length. It is 
composed of but four segments, including the 
head. The cephalic extremity, which is pro- 
longed to form a well-marked net, is capped 
by a pointed rostellum. In the center of the 
head are well-marked sucking-cups (Fig. 156). 
The rostellum is surrounded by a double row 
of hooks, numbering between 30 and 40. The 
final segment, when sexually mature, is as long as the three ante- 
rior segments; it is provided with papillae at the margin of the 
proglottis, below the central line. The uterus, which is stuffed 
with ova, may easily be outlined under a two-thirds objective. 

Detection in Man. — The problem of the detection of this 
parasite in man is radically different from that for the detection 
of other tape-worms, because man is the intermediary host, and 
only the head or scolex of the parasite develops. When the 



//•Mv 



r-^Wj^v^ 



mm 



Fig. 156. — Taenia 
echinococcus, enlarg- 
ed. Above, at tiie 
right, echinococcus 
of natural size (after 
Heller). 



TAPE-WORMS. 



405 



scolex develops in the human tissues, 
it forms a lesion known as a hydatid 
cyst. Each larval scolex is provided 
with a crown of hooklets (Figs. 122- 
124). Free hooklets and shreds of 
laminated, finely granular, yellowish 
membrane are usually found in the 
fluid obtained by puncture of these 
hydatid cysts. In searching for the 
products of the Taenia echinococcus a 
low power of illumination is necessary. 
These hooklets and scolices are de- 
tected by placing a drop of the sus- 
pected material upon the center of a 
shde and studying it under a two-thirds 
objective. It is more satisfactory to 
add a cover-glass to such specimens, 
and to bring the individual scolex into 
focus under a one-sixth or one-eighth 
objective, when it will be found to dis- 
play the characteristics set forth in the 
accompanying illustrations. Products 
of the Taenia echinococcus are well 
preserved when mounted in cast med- 
ium, Farrant's medium, and in glyc- 
erin-jelly. 

Clinical Significance. — "This spe- 
cies, in its larval conditions, is prob- 
ably more injurious to the human race 
than all the other species of entozoa 
put together; or, to say the least, it is 
more frequently the immediate cause 
of death than any other internal para- 
site" (Cobbold). 

The finding of hooklets, scolices, or 
membrane of the Taenia echinococcus 
is positive evidence of infection with 
this parasite, and that the larval para- 
site (scolex) has developed within the 
human organism. It is comparatively 
common to find evidence of echino- 



pr 



=« 



f 



Fig. 157. — The mare^inate tape-worm — Taenia mar- 
ginata — common in the dog (natural size) (after 
Stiles). 



Fig- 157- 



4o6 



THE FECES. 



COCCUS infection in the contents of cysts and abscesses of the liver, 
lung, and kidney. The scoHces develop in the brain and men- 
inges, but they are less common. The products of a hydatid 
cyst should always be sought for in the sputum, and I have found 
them twice in the urine (page 292). 

Taenia Marginata. — This parashe (Fig. 157), a species 
common to the dog, has been known to infest man in but few 
instances. 

Hymenolepis Nana. — The Hymenolepis nana (Taenia nana), 

or dwarf tape-worm, is occasionally 
encountered in the intestinal canal of 
man, but is far more common in the 
intestine of the lower animals. This 
parasite is rare in America, but com- 
mon in Italy, Egypt, and along the 
Mediterranean. Young individuals 
are oftenest infected, and display the 
general symptoms caused by other 
tape-worms. In length the Hymeno- 
lepis nana will be found to vary be- 
tween two and four inches (Fig. 158). 
Its characteristic outhne, except its 
head, is practically that of the larger 
tape-worms. 

Head. — The head of the Hymeno- 
lepis nana differs radically from the 
heads of other tape- worms herein des- 
cribed, since it is more or less pear- 
shaped and displays four suckers and 
a club-shaped rostellum (Fig. 158). It 
also contains from 24 to 30 booklets, 
which are arranged in a single row to 
form a crown at the anterior portion 
of the head. I recovered at postmor- 
tem 96 worms (Hymenolepis nana) 
from the intestinal canal of a cat that 
had been used for experimental feed- 
ing. All these worms were alive when 
removed from the cat, and while yet warm, many of them were 
studied microscopically. About half the number of parasites 
showed the club-shaped rostellum projected from the head, yet 
the accompanying illustration, which was made six hours later, 
does not show this condition. 

Proglottides and Ova. — The proglottides of the Hymenolepis 



^ 


^ 




<tiy^^'^ %$^'.' 


'/'l^v 




'vkJ 


— 7 




\ 


1 




] 


\ 

\ 

\ 


1 


;.'-, 


r 
1 

/ 


\ 

\ 




/ 


\ 




/ 
) 
. ( 


( 1 




V 







Fig. 158. — Hj-menolepis nana 
from intestine of a cat (personal 
observation) : i, Head and neck 
(obj. B. and L. two-thirds) ; 2, head 
and neck (natural size) ; 3, largest 
segments (natural size). 



TAPE-WORMS. 407 

nana are described by the accompanying illustration. The ova 
are numerous and are slightly opalescent, oval bodies enveloped 
in a rather distinct membrane. These ova measure from 0.039 
to 0.060 mm. in diameter. In my series of studies I was unable 
to distinguish satisfactorily an embryo within this capsule, although 
a six-hooked embryo is said to occupy each mature ovum. 

Infection with the Hymenolepis nana is supposed to occur 
through the eating of certain snails in which the cysticercus form 
of the parasite develops. 

Taenia Cucumerina. — Under this caption has been described 
a dwarf tape-worm which resembles in many respects the Hym- 
enolepis nana. This parasite is said to infect children and the 
lower animals, especially the cat and the dog. It resembles the 
Hymenolepis nana in that it displays a well-marked rostellum 
around which the booklets are arranged in rows. In two speci- 
mens of tape-worm determined to be the Tasnia cucumerina 
and recovered by me from the intestine of a cat it was difficult 
to detect any marked difference between these parasites and the 
specimens of the Hymenolepis nana. The cysticercus form of 
the Taenia cucumerina is said to develop in flies. 

Taenia Flavopunctata (Hymenolepis diminuta). — This is a 
rare intestinal parasite of man. It was first described by the late 
Dr. Leidy as occurring in the human feces. In 1900 an elaborate 
study of this parasite, with the report of a ninth case of infection 
in man, appeared from the pen of the late Dr. Frederic A. Pack- 
ard.* 

In length this parasite will be found to vary between 25 and 60 
mm. The head is provided with two rather well-marked sucking- 
cups. The ova are quite similar to those of the Taenia solium. 
The cysticercus form of the parasite develops in cocoons and 
certain caterpillars. 

Dipylidium Caninum. — The Dipylidium caninum, or double- 
pored dog tape- worm, belongs to a family of intestinal para- 
sites rarely encountered in man, but common to the cat and 
dog. Dr. Charles Wardell Stiles, in addition to reporting an 
example of infection in a child, has described this parasite in 
detail.f The parasite is best described by the accompanying 
illustrations, taken from Stiles (Figs. 159, 160). Its segments, which 
are elliptic, elongated, tape-like bodies, need not in any way be 
confused with those of other intestinal parasites (Fig. 150). The 
adult parasite commonly infests the lower animals, as above 
mentioned, and the larval stage of the worm develops in lice and 

* "Jour. Amer. Med. Ass.," Dec. 15, 1900. 
t " x\mer. Med.," Jan. 10, 1903, p. 65. 



4o8 THE FECES. 

in fleas (Fig. i6i). Stiles states that the Dipylidium caninum is 



y 



1 ^\t 1 



N^V-^- 




'^ " ^i \ 5 ^ *^ \ 



tcca 




one of the smaller tape-worms, but should be looked upon as a 
pathogenic parasite, and that it sometimes burrows into the 



TAPE-WORMS. 



409 



intestinal mucosa. The head of the parasite shows four sucking- 
cups and a rostellum which is surrounded by four rows of hook- 
lets. 

Ova. — A microscopic examination of the feces does not yield 
positive information in all cases of infection with the Dipyhdium 
caninum, since ova are not always present, and when present, are 
of small size and may be but few in number. In this respect 
infection with the Dipylidium caninum differs radically from in- 
fection witli the Taenia solium. 
Taenia saginata, and the Diboth- 
riocephalus latus. 

The individual ovum of Dip- 
ylidium caninum is Avidely differ- 
ent from that of any other form 
of tenia loiown to infest man. 
"In the genus tenia we find a 
thick, striated inner shell (em- 
bryophore), while in dipylidium 
the inner shell is thin" (Stiles). 
A six-hooked embryo is to be 
obsen-ed in each egg (Fig. 161). 

Taenia Madagascariensis 
(Grcnet). — A form of tape-worm 
which has been found to infest 
man residing on the eastern 
coast of Africa. This parasite 
may attain a considerable length 
and its segments reach a maxi- 
mum number of 600. The dis- 
tinctive features of this para- 
site are trapezoid segments; a 
double row of hooklets sur- 
rounding its rostellum, and its 
well-defined sucking-cups. Its intermediary host is unknown. 

Taenia Africana. — A parasite detected in the human intestine 
of man. The host had resided in the vicinity of Nyasa Lake. 
Linstow* reports the parasite as being devoid of hooklets. It 
may vary greatly in length, and its segments are broader than 
they are long, and are usually stuffed with ova. The branches 
of the uterus are not divided dichotomously. 

A Questionable Intestinal Parasite. — Numbers of the 
following described parasites have been found in the feces of 
several cases of epilepsy. I am not aware that this parasite has 

* "Cenlralbl. f. Bakt. u. Parasit.," 1900, vol. xxviii, p. 485, 




Fig. 160. — Head of Dipylidium caninum, 
showing four rows of rose-thorn hooks on 
the rostellum and four unarmed suckers 

(Stilesj. 



410 



THE FECES. 



been recovered from the human feces except in the United States 
along the tributaries of the Mississippi River. This parasite has 
been studied by G. H. French.* 

The adult worm is translucent, measures about J inch in 

length, and is shown in the 



Fig. 6. 



Fig. 7. 




Fig. 161. — Fig. 5, Egg packet of Dipylidium 
caninum ; Fig. 6, egg of same — six-hooked embrjo 
(after Stiles) ; Fig. 7, Cryptocystis tricodectis, as 
found in the flea (after Leuckart). 



accompanying illustration 
(Fig. 162). Its anterior 
end bears two black hooks 
which are slightly diver- 
gent, and beneath these 
hooks is a black central 
hne, a suggestion of an 
enteric canal. The ec- 
toderm is distinctly 
divided into twelve seg- 
ments, but no correspond- 
ing markings are sho\^TL 
in the endoderm. The 
incisures, with the excep- 
tion of the first three, 
have a band of short 
spines that project back- 
ward. The posterior seg- 
ment is somewhat villous at the end. A cluster of spines is 
also seen beneath the points of the hooks. French declines to 
classify this parasite. 

Helophilus. — The helophilus or eristalis (Fig. 163) was 
recovered by me from the feces of a child which had been in 
rather ill health for some 
weeks. During this illness 
the child had become mark- 
edly nervous, and had also 
experienced slight convul- 
sions. The mother claimed 
that the child had passed 
from one to twelve parasites 
at each bowel movement for 
a period of several weeks, 
that the specimen from which 

the accompanying illustration (Fig. 163) was made was a fair 
representative of the worms previously passed. 

The parasite was determined by Dr. Ch. Wardell Stiles, 
Bureau of Animal Industry, Washington, D. C, who writes me in 

* "Jour. App. Mic," Rochester, Dec, 1900, p. 1089. 




Fig. 162. — Parasite from feces in a case of 
epilepsy (after G. H. French). 



TREMATODES OR FLUKES. 



411 



part as follows : ' ' The specimen which you sent me for determina- 
tion ... is the larval stage of some insect, probably a 
species belonging either to the genus Eristahs or Helophilus." 




Fig. 163.— Helophilus or eristalis (recovered from feces of a child— an epileptic). 



Blue-bottle Fly. — The larvae of this insect (Fig. 164) are 
often found in the feces of man residing in tropic districts. This 
ringed, cylindric parasite is from J to i 
inch long, and its body is covered with fine 
spines or hairs. 

Neven-Lemaire* mentions nineteen spe- 
cies of diptera whose larvae may be found 
in the intestine or the feces of man. 



TREMATODES OR FLUKES. 

Fasciola Hepatica. — The common Hver 
fluke is best described by the accompanying 
illustration (Fig. 165). At its tapering ex- 
tremity (head) the parasite is provided with a 
single sucker. A second sucker is at times 
detectable upon the ventral surface, and situ- 
ated between these sucking-cups is to be seen 
the genital opening which leads to the uterus. 

The ova of this parasite are ovoid in con- 
tour and measure about 0.13 by 0.8 mm. 
These ova are brown in color, and are pro- 
vided with an apparent lid at one extremity 
(Fig. 165). This parasite is not uncommon 
in sheep, swine, and other animals, as well as in man. 
instances the ova appear in the feces. 

* " Parasitologic Animale." 




Fig. 164.- 
the blue-bottl 
ca vomitoria 
in feces (aft 
art). 



-Larvae of 
efiy (Mus- 
) as found 
er Leuck- 



In rare 



412 



THE FECES. 




Fig. 165. — I, Narrowliver fluke — Fasciolahepatica 
angusta (after Stiles). 2, Egyptian liver fluke — Fas- 
ciola hepatica aegyptiaca. 3, Common liver fluke — 
Fasciola hepatica (after Stiles). 4, Large American 
fluke — Fasciola magna (after Stiles). 5, Ciliated 
embryo (miracidium) of large American fluke within 
egg-shell (after Stiles). 6, Egg of large American 
fluke showing germ-cells surrounded by large number 
of vitelline cells ; egg-shell provided with a cap. 7, 
Lancet fluke — Dicrocoelium lanceatum (after Stiles). 
8. Egg of lancet fluke with embryo (highly magni- 
fied) (after Leuckart). 



Dicrocoelium Lance- 
atum {Lancet Fluke).— 
The Dicrocoelium lance- 
atum is a parasite which 
rarely infests man, and, 
SO far as I am aware, has 
been detected only along 
the Baltic Sea. It will 
suffice to say that this 
parasite closely resembles 
the Fasciola hepatica, 
except that it is much 
smaller (Fig. 165). Its 
ova are also quite small 
(Fig. 165), and are said 
to contain well-developed 
embryos. 

Fasciola Hepatica 
Angusta {Narrow Fluke). 
— This parasite is probably 
a variety of the liver fluke 
common to man (Fig. 165). 
It has been found in cattle 
slaughtered at St. Louis. 
Blanchard regards this 
form as identical with 
Fasciola gigantica. 

Fasciola Hepatica 
-^gyptiaca {Egyptian 
Fluke) . — The Egyptian 
Hver fluke is also to be 
considered in a study of 
the trematodes known to 
infest the human liver and 
bile-passages. This para- 
site has been recovered 
from the giraffe, and ques- 
tion has arisen as to 
whether or not the Egyp- 
tian fluke is identical with 
the narrow fluke, Fasciola 
hepatica angusta, previ- 
ously described. Cattle 
and man are also probable 
hosts for this parasite. 



TREMATODES OR FLUKES. 



413 




Fig. 166. — Eggs of Distoma hepati- 
cum and Distoma lanceolaturn, mod- 
erately magnified (Heller). 



Fasciola Magna {Large American Fluke). — According to 

Stiles, the large American fluke (Fasciola magna, Fig. 165) is ap- 
parently more common in the United States than is the common 

liver fluke (Fasciola hepatica). According to Dinwiddle, in 

certain sections, particularly in 

Arkansas, a large percentage of 

the cattle are infected with this 

organism. Bassi noted that this 

parasite caused a fatal disease in 

deer. I recovered three specimens 

of this parasite from the liver of a 

Virginia deer. 

Distoma Sinense (Opisthorcis 

sinense). — MacConnell was the 

first one to describe the Distoma 

sinense as infecting man in the East 

Indies. At present this parasite is 

rather generally known throughout 

Japan, Corea, Formosa, and China. 

The Distoma sinense varies in 

length from 20 to 22 mm., and 

is leaf-shaped. This parasite is of a reddish shade and, at times, 

fairly translucent. 

The ova vary in length from 28 to 30 /^, and are from 15 to 17 // 

at their greatest breadth (Fig. 167). In each ripe ovum it is pos- 
sible to detect a ciliated embryo. 

Clinical Significance. — According to Manson, the Distoma 
sinense invades the bile-ducts and the gall- 
bladder, causing a thickening of the bihary 
canals, which become greatly expanded in 
places to form diverticula. In these cavities 
numbers of parasites are to be found. Each 
diverticulum communicates with a bile-duct. 
The ova (Fig. 167) and rarely the adult para- 
sites may escape through the bihary canals 
into the intestine and appear in the feces. 

Baels states that in the low, marshy dis- 
tricts of Japan, where the hygienic surround- 
ings are especially bad, he found 20 per cent. 

of the population to be infected with this parasite. Diarrhea 

and recurrent attacks of jaundice are prominent features of the 

disease. 




Fig. 167.—^ 
of Distoma sinense ; b 
parasite, natural size (!' 
A'lajison). 



414 THE FECES. 

ROUND-WORMS. 

Ascaris Lumbricoides. — The Ascaris lumbricoides is readily 
detected, when present in the feces, from the fact that it resembles 
closely the ordinary earth-worm (Plate 26). Ascaris lum- 
bricoides infests the small intestine, but under rare conditions 
it may enter the common bile-ducts, the gall-bladder, stomach, 
mouth, nasal cavity, and appendix. In three specimens of vomitus 
collected from as many patients I found this adult parasite present. 
Specimens of Ascaris lumbricoides will be found to vary greatly 
in size, the female being by far the larger and displaying certain 
characteristics shown in plate 26. This parasite is found most 
often in children, and occasionally the worm may escape from the 
rectum independent of the bowel movement. Cases are recorded 
where the parasite has crawded from the mouth and from the 
nose of a child during sleep. 

Ova. — Ova of the Ascaris lumbricoides are to be obtained 
from the material collected by the introduction of a catheter into 
the rectum (see Ameba, page 388). The individual ovum is of a 
yellowish-brown color, nearly round, and varies from 0.06 to 0.07 
mm. in diameter; and when studied under a one-sixth or a one- 
eighth objective, will be found to display a more or less well- 
marked double outhne (Plate 26). In certain instances the ovum 
will be found to contain a well-defined embryo (Plate 27). The 
shell of these ova is hard and very resistant. 

Ascaris canis. — The Ascaris canis (A. mystax) resembles in 
many respects the Ascaris lumbricoides, but is much smaller (Plate 
26). When placed under a low-power objective (two-thirds), the 
head of the Ascaris canis is found to present a fan-like projection 
from each side, a feature which distinguishes the adult Ascaris 
canis from the smaller Ascaris lumbricoides. The adult female 
Ascaris canis will be found to vary from 100 to 120 mm. in 
length. The male worm is about one-half this size. 

Ova. — Ova of the Ascaris canis resemble to some extent 
those of Ascaris lumbricoides, and are best described by the ac- 
companying illustrations. It is not rare to obtain the Ascaris 
canis from the intestine of the cat at postmortem. 

Oxyuris Vermicularis. — The Oxyuris vermicularis infests 
the lower portion of the intestine and the rectum, and occasionally 
migrates to the vagina and bladder. Children are more often 
affected than are adults. I have records of fourteen cases of 
infection occurring in persons beyond the age of forty. It is 
usually possible to collect the worms from the anus of the 



PLATE 26. 




I, 2, and a. Ascaris lumbricoides: i, Male; 2, female; a, ova. 

3, 4, 5, b, h', h" . Ascaris canis: 3, Male; 4, female; 5, head of female (magni- 
fied); &, ovum; h' , ova, showing segmentation; h" , ova showing embrvo (Kob- 
bold). 

6, 7, 8, and c. Oxyuris vermicularis: 6, Male and female (natural size) ; 7, male; 
8, female (magnified); c, ova (personal observations) (obj. B. and L. one-sixth). 

9 and d. Trichocephalus dispar: 9, Female (magnified); d, ova (obj. Queen 
one-sixth). 



PLATE 27. 




I. Egg of common Ascaris lumbricoides (superficial focus; Stiles). 2. Same, 
median focus greatly enlarged (Stiles). 3. Free embryo, common Ascaris lum- 
bricoides casting its skin (Leuckart). 4-9. Embryology of Ascaris lumbricoides, 
after egg is deposited in feces (Leuckart). 10. Ovum of Oxyuris vermicularis, 
showing embryo (Leuckart). 11. Full-grown free embryo of oxyuris (Leuckart). 
12. Egg of pork tape-worm (Taenia solium) without primitive vitelline membrane, 
showing striated embryophore (Leuckart). 12. Egg of same, with primitive 
vitelHne membrane. 14, 15. Egg of beef tape-worm (Leuckart). 16. Egg of 
Hymenolepis nana (Ransom). 17. Egg of the Dibothriocephaius latus, showing 
lid. 18. Egg of same, highly magnified. 



ROUND- WORMS. 415 

patient, and when thus collected and placed in warm water, 
they will live for a number of days. 

The female worm will be found to measure between 5 and 10 
mm. in length, and the male is scarcely more than half this size. 
From the sides of the head of the oxyuris there is a peculiar pro- 
jection (Plate 26). The extremities in the male and female para- 
site are decidedly different (Plate 26). It is claimed that the 
female parasite locates in the cecum prior to impregnation; but 
my own observations do not coincide with this statement. In 
every case of pruritus ani observed resulting from oxyuris infection 
I have found both male and female parasites present; and many 
of the female parasites were not fully matured and their uteri not 
filled with ova. 

Ova. — A most interesting study is to place the female worm 
upon a previously warmed shde; add sufficient Water partially to 
cover her, and then examine under a low-power objective (two- 
thirds) . The rhythmic contractions of the uterus are in this way 
seen, and with each contraction one or more ova escape from the 
vagina. At times many ova are expelled at a single contraction 
of the uterus, and these are often entangled in a net-work which 
resembles a fish's spawn. To obtain ova of the oxyurides for lab- 
oratory study place several adult female worms in a small bottle ; 
add one or two ounces of water, cork with cotton, and place at 
incubating temperature for from twelve to twenty-four hours. Lift 
the sediment from the bottom of this bottle into a pipet and place 
a drop of it upon the center of a shde; add a cover-glass and 
examine under a one-sixth objective, when numbers of ova will be 
seen (Plates 26, 27). 

The ovum of the oxyuris is about 0.05 to 0.03 mm. The 
operculum, or envelop of this ovum (Plate 27), is thin and asym- 
metric, one side being nearly straight. It is possible to detect in 
some of the ova a rather clearly formed embryo. 

Ova of the oxyuris are common in the feces of children 
infected with this parasite, and I have repeatedly found them in the 
vaginal secretion and in the urine of such children. 

Uncinaria (Ankylo stoma) . — This parasite invades the intes- 
tine of man, and as a result of such infection a group of symp- 
toms are produced which are spoken of collectively as uncinari- 
asis, ankylostomiasis, or hook-worm disease. The total length 
of the female worm will vary between 10 and 18 mm., while the 
male worm is but slightly more than one-half this length. The 
tapering condition of the neck and head, which is shghtly turned, 
is described by figure 168, as is also the tail of the female worm, 
which tapers gradually, terminating at a slightly rounded point. 



4i6 



THE FECES. 



The naked-eye appearance of the Uncinaria americana and 
the Uncinaria duodenale (old-world hook-worm) is quite like 
that of the oxyuris, but when studied under a two-thirds ob- 
jective, both the head and the tail of the uncinaria will be found 
to differ radically from those of the oxyuris. These features are 
made plain by the accompanying illustrations. The tail of the 
male parasite displays several distinct ciha, or hairs (Fig. i68), 
and a three-lobed bursa which serve to differentiate the uncinaria 
from other intestinal parasites. The mouth of the uncinaria is 
also quite characteristic (Fig. i68). The uterus of the female 
worm is readily outlined with a two-thirds objective, and when 




Fig. i68. — Uucitiaria americana : i, Female, natural size ; 2, head ; 3, tail ; 4, ovj 
(B. and L. obj. , eye-piece 2). 



studied under a slightly higher power objective (one-sixth), is 
seen to be filled with ova (Fig. i68). 

Detection in the Feces. — Uncinariasis may exist for a long 
time and yet there be no parasites in the feces. In such 
instances it becomes necessary to administer some drug for the 
purpose of expelling these parasites from the intestinal tract. 
Before the administration of an anthelmintic it is well to give 
the patient sufficient citrate of magnesia to empty the bowel 
thoroughly. The stomach must also be empty. The drug which 
serves best for the expulsion of the uncinaria is thymol, which can 
be administered in doses of 2 gm. (31 gr.) at 8 A. m. and this dose 
repeated at 10 a. m. 



ROUND- WORMS. 417 

Caution. — It is necessary that a careful watch be kept over the 
patient after the administration of the first dose of thymol, since 
this drug often acts as a decided cardiac depressant. Whenever 
its depressing effects are evident, the heart should be stimulated 
with strychnin or alcohol (alcohol is said to favor the absorption 
of thymol by the system). The administration of the drug is not 
to be continued in such instances until the heart has first been 
strengthened by proper cardiac stimulants. 

Two hours later — 12 o'clock m. — follow the last dose of thymol 
with a liberal dose of magnesium citrate or of castor oil, and collect 
all the feces. Worms are found in the stools in from eight to 
twelve hours after the administration of thymol. Add water to 
the feces, mix thoroughly, and strain through gauze, as described 
under the Detection oj the Tape-worm^s Head, page 397. In this 
manner it is very easy to detect the worms upon the gauze, from 
which they should be removed by the aid of a small needle and 
placed in water. These worms are well preserved in 70 per cent, 
alcohol; and when dehydrated, may be mounted in Canada 
balsam. The worms are well preserved after treatment with 50 
per cent, alcohol when mounted in cast medium. 

Ova of the Uncinaria duodenale are to be found in the mucus 
obtained by introducing a catheter into the rectum, and are also 
to be recovered from the feces. The number of ova present in the 
feces is in direct proportion to the number of parasites in the 
intestine, yet Ashford states that the feces may contain great 
numbers of ova when there are but few female worms in the in- 
testine. Ova, when present in the feces, are detected by placing 
a small portion of the dejecta in a glass and adding to it a rather 
liberal quantity of water, mixing thoroughly, and centrifugalizing 
a quantity of this mixture. Sediment collected in this manner 
and studied under a two-thirds objective will be found to contain 
ova. Washing of the feces may be of service (page 387). 

Ova. — ^The ovum of the uncinaria (Fig. 168) measures be- 
tween 0.05 and 0.06 mm. in length by 0.03 to 0.04 mm. in 
breadth. It is common to see ova rather dark and slightly granular 
in appearance while others are faintly opalescent. A third variety 
of ova may be almost hyaline, except for a small portion extending 
along one side of the capsule, where a faintly granular body is 
seen — an apparent embryo. Ova showing segmentation (Fig. 171) 
are extremely common. When the feces is allowed to stand at 
incubating temperature, the embryos are seen to develop rapidly, 
and some will have escaped from their ova in from twenty-four 
to forty-eight hours. The finding of shells of ova showing a 
slight line or opening is at such times very common (Fig. 171). 
27 



4i8 



THE FECES. 



The embryos are said to be found in the feces, but personally I 
have never been able to detect these embryonic worms in such 
feces. 

In mounting ova of the Uncinaria duodenale and americana 
the feces should be diluted liberally with water and the process of 
centrifugalization be repeated three or more times, transferring 
the sediment to a clean tube after each centrifugalization. 
Ova when washed in this manner should be placed upon the 
center of a slide and permitted to dry in the air. They may 
now be mounted in Canada balsam, cast medium, or glycerin- 
jelly. I have in my possession several slides thus mounted in 




Fig. 169. — Section of adult Uncinaria ankylostoma, uterus containing ova (obj. Queen 

one-sixth ; eye-piece 2). 



1896 and at present these ova show well their characteristic 
features. The ringing of the specimen with microscopic asphal- 
tum is not an absolutely necessary step in this technic, yet it is 
my custom to ring all specimens (page 28). 

Clinical Significance. — The detection of either the adult 
parasite or of its ova in the feces is positive evidence of infection 
with uncinaria. B. K. Ashford has shown that a large percentage 
of cases of anemia studied by him in Porto Rico were caused by 
infection with the Uncinaria duodenale (see Blood, page 143). 

Trichocephalus Dispar. — The Trichocephalus hominis is a 
member of a family of trichotrachelides (Plate 26), and inhabits 



ROUND-WORMS. 



419 



the cecum in man. This parasite will be found to vary between 40 
and 50 mm. in length. 

Ova. — The ovum of the trichocephalus is of nearly the same 
size as the ovum of the uncinaria, and measures about 0.05 mm. 
in breadth by 0.06 mm. in length. The ovum of the trichocephalus 
is unlike that of other intestinal parasites, since it displays a 
decided double outline upon each lateral border (Fig. 171). 
Another feature which serves to distinguish this ovum is the fact 
that it displays a hyahne or slightly 
yellowish lid at each extremity. The 
central portion of the ovum is coarsely 
granular, as a rule, and in some of the 
specimens there is seen evidence of 
segmentation. 

Ova of the Trichocephalus dispar 
may be mounted in the manner des- 
cribed for mounting the Uncinaria 
duodenale. It is claimed for the 
Trichocephalus dispar that it is to 
be found throughout the civihzed 
world. 

Clinical Significance. — In the feces 
from all cases of infection with the 
Uncinaria duodenale I have found 
ova of the trichocephalus. Ashford 
has informed me that these ova are 
always present in the feces of persons 
suffering from uncinariasis, and that 
the degree of anemia caused by the tri- 
chocephalus remains an open question. 
Upon two occasions I have detected 
ova of the trichocephalus in the urine, 
and they are commonly met with in 
the feces of typhoid fever and of dys- 
entery. 

Strongyloides Intestinalis.— 
Specimens of the Strongyloides intes- 

tin^hs are commonly found in the feces of persons residing in 
China and in tropic and subtropic districts. Of recent years 
this parasite has been found in southern United States. Thayer 
contributed an admirable monograph on this subject.* 

The length of the adult female worm is about i mm. and its 
greatest breadth about 0.04 mm. The head tapers slightly, and 
the tail terminates in a fine point. In the living parasite there are 
to be seen slight transverse furrows. The mouth displays three 

* "Jour, of Exp. Med.," Nov. 29, 1901. 














^! 


ii 




\i\ 


1 




f. 


^ 




/ 



Fig. 170. — Two larvae of old- 
woild hook-worm, end of second 
stage (after Perroncito). 



420 



THE FECES. 



distinct lips, and is continuous with a triangular esophagus which 
becomes constricted. Beyond this, constriction is again expanded 
to form an ovoid enlargement. The uterus is readily outhned, 
and is slightly posterior to the center of the body, on the ventral 
surface of which is a small opening which leads to the uterus. 
Price* states: ''In some instances the young had actually broken 
the shell and were seen in the uterus, though more often the ova, 
on deposition, contained well- formed motile embryos." 

The male parasite is slightly smaller than the female (Plate 28). 
The peri-intestinal cells are accompanied by what appears to be a 
long gland composed of small globules. This gland, probably 
a testicle, extends to the base of the tail, where it terminates in 




Fig. 171. — I, 2, Ovum of Trichocephalus dispar at different focus ; 3, Trichocephalus dis- 
par containing- embryo ; 4, ovum of Tricliocephalus dispar (obj. B. and L. one-twelfth oil-im- 
mersion); 5-9, ova of the Uncinaria americana (new-world hook-worm) from feces; 10, 
No. 6, X 1000; II, degenerated ovum of Uncinaria duodenale ; 12, o\um of old-world hook- 
worm, showing rupture of shell ; 13, empty shell ; 14, shrunken empty shells (all from personal 
observations); 15, escaping embryo (after Perroncito); 16, Uncinaria duodenale, male and 
female, natural size (after Stiles). 



two horn-like spicules. These worms are to be found postmortem 
in the duodenum, jejunum, and occasionally in the ileum. They 
at times migrate to the stomach, even under apparently normal 
conditions, and have been found in the vomitus following the 
administration of an emetic. They are also to be found in the stools. 
When the stools are kept warm for a variable period, they will be 
found to contain an embryonic parasite which is much longer, 
thinner, more homogeneous, and more active than is the- or- 
dinary rhabditiform embryo fFig. 172). This parasite is the 
strongyloid in its embryonic state. The parthenogenetic female 
worm (capable of production for several successive generations 

* "Jour. Amer. Med. Ass.," Sept. 12, 1903, p. 651. 



ROUND- WORMS. 



421 



without renewed fertilization by the male) also displays a strongy- 
loid type, and possibly develops directly from this strongyloid 
embryo. The strongyloid embryo, while longer than the rhabditi- 
form, does not attain the size of the parthenogenetic mother- 
worm. Price has offered the following table of measurements: 



Rhabditiform. Filariform. 

Length o.;^7,o mm. 0.50 mm. 

Breadth 0.022 mm. 0.02 mm 



Free 
Sexually. 

1. 00 mm. 
0.04 mm. 



Parthenogenetic 
Mother-worm. 

2.20 mm. 
0.03 mm. 



The ova of the Strongyloides intestinalis resemble in certain 
respects the ova of the uncinaria, and 
measure from 60 to 70 /j. by 35 to 39 /i. 

Strongyloides Subtilis. — Strongy- 
loides subtilis is generally known as an 
Egyptian and Japanese strongle. In 
view of our tropic possessions and the 
frequency with which persons travel in 
Japan and Egypt, the possibility of this 
parasite becoming fairly common in 
Americans is increased. It has not 
been proved, however, that the Strongy- 
loides subtilis (Plate 28) has not a far 
wider geographic distribution. 

Recognition. — In a general way, 
according to Stiles, strongyhd^ may be 
determined by the following character- 
istics: "Body slender; anterior extremity 
occasionally with alae. . . . Mouth 
small, without teeth; lips soft, often 
indistinct, papillae very small. . . . 
Bursa (male) entire or excised ventrally, 
in some cases bi-, tri-, or multilobed; 
spicules 2, often with accessory piece." 
The uterus displays two horns, and the 
vulva is, as a rule, situated in the 
caudal half of the body. This para- 
site will be found to vary between 4 and 
7 mm. in length ; its oral papillae are not 
conspicuous, and its cuticle displays fine 
transverse striations; longitudinal lines 
are also present. The lateral longitu- 
dinal hnes are more distinct than are 

the central hnes. The male parasite is considerably the smaller 
and seldom exceeds 5 mm. in length. 




Fig. 172. — I, Egg of the Cochin 
China diarrhea worm (Strongy- 
loides stercoralis) ; 2, rhabditi- 
form embryo of same ; 3, filari- 
form larva of the same (after 
Thaver) (see also Plate 28). 



422 THE FECES. 

Ova. — The ova of the parasite are oval in contour, and, accord- 
ing to Stiles, measure about 63 by 40 fi ; the shell is thin, and the 
Qgg contents are highly granular. Segmentation is not seen in 
the ova obtained from parasites of a human host. It has not been 
proved that the detection of the ova in the feces is practical, since 
it is thought they occur only where a severe grade of infection 
exists. 

Anguillula Intestinalis. — Ova of the x\nguillula intestinalis 
are seldom to be found in the feces, but the embryos of this parasite 
are commonly found in the dejecta. The ova, when present, are 
slightly longer than are the ova of the uncinaria, more elliptic, and 
decidedly more tapering at their poles. The adult worm may 
appear in the feces. 

Trichinella Spiralis. — The Trichinella spirahs is introduced 
into the system through the ingestion of infected meats in which the 
embryo worms are encysted. The first symptom.s of infection with 
the trichinae that concern us from a clinical standpoint are those 
of gastro-intestinal irritation — -nausea, vomiting, and diarrhea. 
These symptoms do not appear until about one week after the 
taking of infected meats. I have found these symptoms to appear 
in a shorter period (three days) where an animal had been fed a 
large amount of measly pork. It is the rule for these symptoms 
to be rather mild in man, and for the disease to progress to the 
stage where the embryos become lodged in the muscle-tissue before 
it is recognized. Trichinosis is a not uncommon disease through- 
out Europe and in America. 

Feces. — The feces, when collected during the paroxysm of 
gastro-intestinal symptoms, may at times contain the adult 
trichinae (Fig. 173); and the detection of this parasite in the feces 
differs in no way from that outlined for the detection of the 
Uncinaria duodenale. 

Embryos. — Embryos of the Trichinella spiralis are found in the 
muscles in practically all portions of the body. The accompanying 
original illustrations (Figs. 174, 175) were sketched from portions 
of muscles recovered upon the twenty-first day and during the 
seventh wxek after the first symptoms of the disease, and figure 
176 was obtained one year later. 

Detection. — In man a most favorable point of election is the 
outer head of the gastrocnemius or the tendinous portion of the 
soleus muscle. An established fact is that the larvae are far more 
numerous near the tendinous insertions of the muscles. 

1. Cleanse the skin overlying these tendons as though pre- 
paring for any surgical operation. 

2. Inject into the skin a few drops of a 4 per cent, solution of 



PLATE 28. 




Strongylus Subtilis. 

1. Full-grown male. 

2. Female. 

3. Spicules of male with trowel-shaped accessory spine. 

4. Transverse section through middle of esophagus. 

5. Anterior, 6, posterior section through vagina. 

7. Transverse section through distal part of vagina. 

8. Anterior end of female (all greatly enlarged) (Looss). 



ROUND-WORMS. 



423 



cocain hydrochlorate. The deeper structures may be injected 
down to the sheath of the muscle, but in most instances deep 
injection is not required. 
In from two to five minutes 
anesthesia will be found 
to be complete. 

3. Make an incision 
two or three inches long 
directly over the tendin- 
ous portion of the muscle, 
dividing the skin and fas- 
cia until the sheath of the 
muscle tendon is exposed. 
Grasp the sheath of the 
tendon with a rat-toothed 
forceps, make a longi- 
tudinal incision into the 
sheath, and keep the 
sheath separated by grasp- 
ing each margin of the in- 
cised sheath with a forceps. 
Take up a small portion of 
the muscle-tissue and dis- 
sect it away with the aid 
of a scissors. 

4. Place this small bit 
of muscle-tissue in a glass 
containing warm water. 

Caution. — Should the 
muscle be placed in gly- 
cerin or in alcohol, the 
movements of the trichinae 
are arrested. 

5. Close the wound 
with two or more sutures, 
and dress aseptically. 

By this method suffi- 
cient muscle can be re- 
moved for chnical study without danger to the patient, 
plunging of a harpoon into the muscle is not advocated. 

Study of the Tissue. — i. Chp a small piece from the mass 
of tissue, always cutting transversely to the muscle-fibers. Place 
this clipping on the center of a slide, add to it a few drops of water, 
and tease the particle of tissue until the fibers are well separated. 




73. — Adult intestinal Trichinella (human); 
male, female, and two embryos, the former natural 
ze, the latter slightly magnified (Birch-Hirschfeld). 



The 



424 THE FECE$. 

2. Without the addition of a cover-glass place the specimen 
under a two-thirds objective and examine for the larval trichina 
(Figs. 174, 175). By the addition of a cover-glass the trichina 
may be studied under a higher power objective — one- sixth or one- 
eighth. 

Trichina are best seen with a low illumination, since the para- 
site is often rendered transparent when the light is too strong. 
In the process of teasing the muscle-tissue certain parasites are 
usually freed from the tissue and appear in Hquid upon the slide 
(Fig. 174). During the first two months after infection with 
Trichinella spiralis the larval parasite becomes actively motile when 
it is separated from the muscle-tissue. It will uncoil and recoil 
itself, allowing its more pointed extremity to remain stationary, 



Fig. 174.— Trichinella spiralis (larvae) Fig. 175. — Trichinella spiralis (larvae) 

from head of right gastrocnemius muscle ; from outer head of left gastrocnemius 

seventh week of disease (Queen two-thirds muscle; twenty-first day after symptoms 

obj.; eye-piece 4). iQueen two-thirds obj.; eye-piece 2). 



while the remainder of its body stretches across the field. When- 
ever this larva comes in contact with any muscle-tissue, it appears 
to cling tightly to it, at once resumes its usual spiral-like position, 
and remains quiescent. In the study of a number of parasites no 
movement was ever detected when the parasite was in contact with 
the muscle-tissue. 

After a variable period of time these larval parasites become 
encysted in the muscle-tissue, and at times appear to be within a 
single muscle-fiber (Fig. 176). Still later the sheath enveloping the 
larvae becomes calcified. I found, by freeing the encapsulated 
trichinae, that it often possesses slight movement, but the decided 
movements displayed by the parasite before encapsulation are 
lacking. I conducted a series of feeding experiments at the Phila- 



ROUND-WORMS. 



425 



delphia Hospital in 1898, and it will suffice to state that cats, rats, 
and white mice are readily infected with the Trichina spirahs. 

Permanent Mounts. — 
When it is desired that per- 
manent mounts be prepared, 
tease" a small portion of a 
muscle-fiber on the center 
of a slide, evaporate nearly 
to dryness, and then add to 
the specimen sufficient cast 
medium, Farrant's medium, 
or glycerin-jelly to cover it 
completely. Then allow a 
cover-glass to fall gently upon 
the medium and specimen. 
Place such mounted speci- 
mens in a cool place for 
twenty-four to forty-eight 
hours, and ring with some 

form of microscopic cement. The specimens from which the 
accompanying illustrations were sketched were mounted in this 
manner seven years ago, and at present they show equally well 
all characteristics of the parasite. 




Fig. 



Encapsulated trichina from muscle 
one year after infection. 



CHAPTER V. 
THE SPUTUM. 

COLLECTION. 

Sputum should be collected in a suitable receptacle, for which 
purpose I find an ordinary vaselin bottle most convenient. This 
should be placed at the patient's bedside or in his room, so that 
at the time of the morning exacerbation of coughing he may 
expectorate directly into the bottle. If possible, the bottle should 
be filled one-half or more with sputum, when it should be corked 
tightly and wrapped in a quite heavy paper, upon which the name 
of the patient is to be clearly written. 




177. — Sputum cup. 



Caution. — Do not add water to the sputum. 

A paper spit-cup has been devised for the collection of sputum 
at the bedside, and is of special value, since it may be burned 
after use. I have found an earthen cup, provided with a concave 
cover in the center of which is a small opening like that in a cus- 
pidor, equally satisfactory. These cups may be disinfected by 
boihng or by strong bichlorid solution, a feature of greatest impor- 
tance in any receptacle used to collect sputum. 

426 



METHOD OF COLLECTING SPRAY. 



427 



METHOD OF COLLECTING SPRAY, 

This is accomplished by means of a mask (Figs. 178, 179), 
made from German-silver wire, one piece of which is molded to 
fit the face, resting on the nose, cheeks, and chin. To obviate any 
irritation to the patient this portion is covered by a piece of 
rubber tubing. Suspended from this wire is a second oblong 
portion provided with two lateral grooves, which serve to accom- 
modate two microscope slides. When the mask is in position, 
the slides are held directly in front of the mouth and nose, at a 
point three inches distant from the lips. The mask is held in 
position by an elastic band which passes above the ears and over 
the occiput (Fig. 179). 

Patients are allowed to wear the mask with the clean slides 
in position for from one to one and a half hours, during the day, 
when they are apt to 
cough least, and are in- 
structed to remove it 
during a paroxysm of 
coughing. It is never 
worn during the morning 
or evening, the object 
being not to collect on 
the shde the spray pro- 
duced by vigorous cough- 
ing, which has already 
been studied, but to 
determine whether or 
not consumptives 
emit a fine spray, 
when talking, laughing, 
clearing of throat, or by 

their characteristic hacking, that was in any way dangerous to 
the health of their associates. 

Fifty patients, 34 males and 16 females, all of which presented 
unquestionable evidence of either pulmonary or laryngeal tubercu- 
losis and in whose sputa tubercle bacilli had been found, were 
mad^ to wear the mask as above described. 

Microscopic Study. — Specimens are fixed and stained by 
carbolfuchsin and Gabbett's acid-blue solution. Of the specimens 
collected from 50 patients, those from 49 were found to contain 
bacteria — the diplococcus and the streptococcus being the most 
constant, yet bacilli and clusters of cocci were not unusual. A 
single minute droplet often contained organisms of each class. 




Fig. 178. — Mask with slides in position. 



428 



THE SPUTUM. 



Of these 50 specimens, 38 were found to contain tubercle 
bacilli in variable numbers, 4 to 6 bacilli being the smallest number 
found in any specimen, and many of the specimens, under a 
one-twelfth oil- immersion objective, showed fields of bacilli too 
numerous to be counted. 

CHARACTERISTICS OF SPUTUM. 

Quantity. — The quantity of sputum ejected during the twenty- 
four hours will be found to vary greatly, and will bear a direct 




Fig. 179. — Patieiu wearing mask. 

relation to the nature of the disease in question. The quantity 
varies from a few cubic centimeters to 500 or even 1000 c.c. a 
day. Profuse expectoration is to be seen in pulmonary hemor- 
rhage, pulmonary edema, bronchiectasis, tuberculosis, rupture of 
an abscess into the lung (diaphragmatic, hepatic, pulmonary), and 
rarely in pleural effusions. The so-called albuminous sputum, 



CHARACTERISTICS OF SPUTUM. 429 

which is observed in gangrene and bronchial blennorrhea, is often 
profuse. In acute processes the sputum is generally scanty or 
moderate in amount. 

Odor. — The odor of the sputum can be regarded as a charac- 
teristic in but two conditions — viz., pulmonary gangrene and 
putrid bronchitis, in which diseases it has a heavy, pungent smell. 
At times an odor resembling that of gangrene, and equally un- 
pleasant, is emitted from the sputum of bronchiectasis. Sputum 
that has been allowed to stand at room-temperature develops a 
decided odor in seventy-two hours. A sweetish odor is often 
emitted by the sputum in cases of pulmonary ulceration, 
bronchitis, and perforating empyema. When tyrosin is present 
in the sputum of empyema, the odor resembles that of rancid 
cheese. In case the odor of tyrosin is detected in the sputum, it 
suggests that some extraneous purulent material has gained 
access to the bronchial tract. 

Consistence and Tenacity. — The density of the sputum 
will be found to correspond more or less closely to the amount, 
and to vary from a watery fluid to that of a gelatinous mass. 
At times, when the sputum is placed in a cylindric glass, it 
wiU be found, upon standing, to have separated into strata, the 
superior of which is covered with a heavy froth or beaded with fine 
air-bubbles. The sputum immediately, and for some distance 
below the froth, will be found clear and of a liquid consistence. 
Below this stratum will be found a layer containing fiocculi and 
particles of mucus; while the lowest stratum, which may at times 
be the deepest and again the shallowest of these strata, is often 
composed of a sediment which is purulent or bloody. Sputum 
may be of a creamy consistence, its color depending largely upon 
the character of the substances of which it is composed. Liquid 
sputum is found in edema of the lungs, tuberculous laryngitis, 
early in pulmonary tuberculosis, perforation of an empyema, or 
of a diaphragmatic or hepatic abscess; and in pulmonary abscess 
and gangrene, in all of which diseases the quantity may be large. 

The exact causes for the high degree of tenacity often displayed 
by the sputum remain undetermined. Mucin, while once regarded 
as an important factor, does not appear to contribute largely to 
this feature, since highly tenacious sputum is known to occur in 
cases in which the quantity expectorated during the twenty-four 
hours is but slight — not exceeding a few cubic centimeters (lobar 
pneumonia). A highly tenacious sputum was observed by me in 
a case in which an amebic abscess had ruptured into a bronchus. 
The tenacity of the sputum is detected by incHning or inverting 
the receptacle into which it has been expectorated. Tenacious 



43° THE SPUTUM. 

sputum shows little or no tendency to flow, but adheres closely to 
the surface of the vessel; indeed, the receptacle with its contained 
sputum may be inverted without danger of spilhng. Such a con- 
dition is rather characteristic of the sputum of croupous pneumo- 
nia before the crisis, and is occasionally seen following an acute 
attack of asthma, as well as in the early stage of acute bronchitis. 

Specific Gravity. — The specific gravity will Hkewise be found 
to fluctuate greatly, and will depend directly upon the general 
character of the sputum. Mucous sputum varies from 1.003 ^o 
1. 01; purulent and bloody specimens vary betAveen 1.014 and 
1.025; ^^'hile serous and highly bloody sputum may reach 1.035, 
but rarely exceed this figure. 

Determination. — The specific gravity of the sputum is best 
determined by placing a quantity of sputum in a bottle the stopper 
of Avhich is held in position by a wire, to prevent evaporation. 
The sputum is then cautiously heated to 60° C. (140° F.), at which 
temperature it is converted into a thin fluid; the specific gravity 
may be taken in the usual manner (see Urine, page 172). 

Reaction. — Sputum is of an alkaline reaction. 

Color. — The sputum will be found to var\' greatly in color 
from that of a perfectly clear, transparent Hquid, through the 
successive shades — gray, yellow, amber, orange, olive green, red, 
chocolate, and black. When the expectoration is entirely mucoid, 
it is colorless and nearly transparent — for example, in the sputum 
of pulmonary edema (when no blood-cells are present) and in the 
so-called "albuminous expectoration." 

The presence of leukocytes in the sputum renders it opalescent 
or turbid, according to the number of cells present ; and the color, 
from the same cause, is first white, then yellow, and, finally, of a 
greenish hue. Green sputum may also be caused by the admix- 
ture of bile-pigments, a not uncommon feature of lobar pneumonia 
when comphcated by jaundice, and by the communication of a 
hepatic abscess with the bronchial tract. The presence of bacteria 
fBacillus pyocyaneus) may be accountable for a green color. In 
cases of amebic abscess, whether hepatic or pulmonary, the sputum 
resembles anchovy sauce in color, as was observed in my private 
practice. 

Black. — Gray sputum may result from the inhalation of 
particles of carbon, while the sputum of coal-miners and those 
residing in the mining districts is often dark and at times black, due 
to the presence of coal-dust (anthracotic sputum, Plate 30). 
Particles of iron may give the sputum a yellow or red color. 

Bloody Sputum. — Sputum tinged with blood and studded 
with minute air-bubbles — "rusty sputum" — is cjuite characteristic 



CHARACTERISTICS OF SPUTUM. 43I 

of lobar pneumonia ; and rusty sputum displaying bloody, punctate 
areas is to be seen in connection with brown induration of the 
lung. Blood gives the sputum a red color, which varies in in- 
tensity with the amount of this tissue added. It is most often 
encountered in pulmonary congestion and in ulceration (phthisis). 
Less frequently hemorrhagic sputum may result from cardiac in- 
sufficiency through an embarrassed pulmonary circulation. When- 
ever the blood is expectorated as soon as it escapes from the vessels, 
it will be found to be of a bright-red color; but retention in the 
bronchi favors the development of a brownish-red, dirty-brown, 
or chocolate-colored sputum. The last is fairly characteristic of 
pulmonary gangrene, although sputum indistinguishable in color 
from that of pulmonary gangrene is to be seen in cases in .which 
large tuberculous cavities exist. Bloody and dark-brown sputa 
are also to be observed in abscess of the lung, as well as in gangrene. 
In these cases the color probably depends upon the presence of 
hematoidin, bilirubin, or both. Prune-juice sputum results when 
blood is retained in an edematous lung; and currant-jelly sputum 
is regarded as suggestive of a malignant disease of the lung. 

Mucous Sputum. — This variety of sputum is clear, sticky, 
tough, and, during the early stage of bronchitis, scant. In the 
later stage of bronchitis pus-cells are added which render the 
sputum more copious and give it a yellowish or a greenish color. 

Mucopurulent Sputum. — This is a variety of sputum seen 
in connection with many forms of pulmonary disease. It is of 
little clinical value except in cases of pulmonary tuberculosis, in 
which, in the event of cavity formation, minute, ragged clumps 
of mucopus which are intimately surrounded by mucus may be 
seen. 

Coin-like masses of sputum {nummular sputum, often regarded 
as characteristic of cavity formation), when first expectorated, 
float upon the surface; but after a time sink to the bottom of 
the liquid, where an aggregation of these coin-hke bodies forms 
a dense, purulent sediment. At times such sputum separates 
into three layers — viz., an upper frothy mucous, a middle serous, 
and a lower purulent layer. In cases of old cavities the sputum 
may -contain grayish- white masses, or, equally important, round 
or irregular particles varying in size from that of a pin's point 
to that of a millet-seed {caseous particles). These usually fall 
through the liquid portion of the sputum and collect at the bottom 
of the vessel; but should they contain air-bubbles, they then pos- 
sess a variable degree of buoyancy and float upon the surface or 
are suspended in the liquid at different depths. Such sputum is 
fairly suggestive of the second and third stages of tuberculosis. 



432 



THE SPUTUM. 



Similar masses have been found in the sputum of healthy indi- 
viduals (rarely), and they are occasionally seen in cases of ton- 
sillitis; but these particles differ from those found in the recent 
sputum of tuberculosis by emitting an unpleasant odor when 
crushed with a needle, and by not containing tubercle bacilH. 

Serous Sputum. — This variety of sputum may be entirely 
distinct from mucous expectoration. It appears as a watery fluid 
which is often blood-streaked. It is fairly characteristic of edema 
of the lungs, and, in the absence of blood-cells, resembles soapy 
water. 



MICROSCOPIC STUDY OF THE SPUTUM. 

With the aid of the microscope positive diagnostic evidences 
are to be obtained from the examination of the sputum. A micro- 
scopic study, on the other hand, is often merely suggestive of the 
existence of certain maladies. 



ORGANIZED CONSTITUENTS. 
Fibrinous Coagula. — During the course of certain pathologic 
conditions an exudate is deposited in the smaller bronchi, and 
after having undergone certain degenerative changes, this exudate 

results in the formation of a complete 
cast of a small bronchus and its branch- 
ing bronchioles, so that a variable area 
of the lung may be involved. During 
the act of coughing a small amount of 
this coagulum, which now forms a 
complete cast of the bronchus, is dis- 
lodged and appears in the sputum as 
a small, gray, white, reddish, yellow, 
mahogany, or bloody particle readily 
detected by the naked eye. Such 
casts may vary from 2 to 10 cm. in 
length and from i to 3 cm. in thickness. 
Detection. — Fibrinous casts may 
be recognized by placing suspicious 
particles of the fresh sputum between 
two slides and making rather firm pressure upon the upper slide. 
The questionable particles are clearly demonstrable when brought 
in focus under a two-thirds or one-fourth inch objective (Fig. 180). 
They appear as fine stems or central trunks from the sides of which 
several smaller casts may be seen extending. From one extremity 




Fig. tSo. — Fibrinous bronchial cast. 



ORGANIZED CONSTITUENTS. 



433 



of the trunk is seen to extend a number of small, twig-like fila- 
ments which divide dichotomously to form casts of the smaller 
bronchi. The diameters of these branches diminish gradually 
and terminate in delicate points. In immediate connection with 
these casts leukocytes, red blood-cells, and epithelial cells may be 
seen, and sometimes Charcot-Leyden crystals (Fig. i8i). 

Clinical Significance. — Fibrinous casts have been found 
in the sputum of fibrinous bronchitis, croupous pneumonia near 
the time of resolution, and in cases in which there is a diphtheric 
process in the finer bronchi. 

Bronchial Spirals. — These bodies, when present in the spu- 
tum, appear to the naked eye much the same as do bronchial 
casts, except that they are 
always white or yellowish in 
color. 

Detection. — T r e a t the 
sputum as described in the 
technic given for bronchial 
casts: at times it will be 
found necessary to use a high- 
power objective (one-sixth to 
one-eighth). Spirals appear 
as faint, translucent, elongated 
masses, with indefinite and 
irregular margins (Fig. i8i). 
A delicate, white, thread- 
like fiber runs longitudinally 
through the center of each 
spiral. This fiber has a tor- 
tuous course, and seems to 
be surrounded by numerous coiled fibrillae. Leukocytes, epithe- 
lial cells, Charcot-Leyden crystals, and, rarely, erythrocytes are 
seen to be entangled in the mass; while surrounding the fibrous 
portion there is a faintly granular hazing. The central thread 
is not discernible in all specimens. 

Clinical Significance. — Spirals are a rather constant find- 
ing in the sputum of persons suffering from asthma, both during 
and after the paroxysmal stage. They are not unusual in cases 
of croupous pneumonia, acute bronchitis, chronic bronchitis, and 
I have observed them in the sputum of cases of tuberculosis, val- 
vular heart disease, diphtheria, and typhoid fever. From their 
mucinous appearance it seems fair to regard them as suggestive 
of a catarrhal process of the bronchi, yet their true formation 
remains undecided. 
28 




Fig. 181. — Sputum from a case of asthma, 
showing Curschmann spirals, Charcot-Leyden 
crystals, leukocytes, and numerous free eosino- 
phile granules ; unstained specimen (Jakob). 



434 



THE SPUTUM. 



Elastic Fibers. — Fibers of elastic tissue may occur in the 
sputum singly, in a more or less perfect alveolar arrangement, or, 
as is most usual, in bundles. They may be demonstrated in the 
manner described for the detection of ''fibrinous coagula," a one- 
eighth objective being used. The method which I have adopted is 
to pour a quantity of sputum in a rather large glass dish, in order 
to secure a thin layer of the sputum, and then to place the dish 
upon a table or any dark background. The more or less soHd 
particles are thus rendered conspicuous, and are transferred to a 




Fig. 



-Fibers of elastic tissue from sputum in a case of pulmonary tuberculosis ob- 
served at Pennsylvania Hospital (obj. B. and L. one-eighth). 



vessel containing a lo per cent, solution of sodium hydroxid, by 
means of a small surgical forceps. Boil the soda solution and its 
contained sputum until a gelatinous mass results or until the 
formed particles of sputum are dissolved; then add four times 
the total quantity of water; place the mixture in a conic glass, 
and allow it to stand for several hours. Remove the sediment that 
has collected by a small pipet, and place it in a centrifuge; add 
water enough to fill the tube and centrifugahze. The sediment 
obtained by the last process may be studied under a one-sixth or 



ANIMAL PARASITES OF THE LUNG. 435 

one-eighth objective, when elastic fibers, if they are present, are 
readily detected (Fig. 182). The addition of a drop of Gram's 
iodin solution to the microscopic specimen facilitates the diag- 
nosis materially. 

Caution. — Boihng with sodium-hydroxid solution, when pro- 
longed, causes swelling, and finally a dissolution of the elastic 
tissue. Attempts to detect elastic tissue without first treating the 
sputum with sodium-hydroxid solution have not been attended 
with satisfactory results by the author. 

Clinical Significance. — The presence of elastic fibers in 
the sputum is suggestive of the existence of a highly destructive 
process in the lung. The true significance of these changes, 
however, is indicated only when they appear in the so-called 
alveolar arrangement, as they commonly do in phthisis and as they 
rarely do in pulmonary gangrene. In the latter condition Traube 
has suggested that elastic fibers may be destroyed by a ferment. 
Elastic fibers are rarely found in connection with abscess of the 
lung, bronchiectasis, and pneumonia. 

Caution. — Direct the patient to wash the mouth and brush the 
teeth carefully before collecting the sputum, to avoid the possible 
expectoration of elastic tissue from retained food-particles. 



ANIMAL PARASITES OF THE LUNG. 

Paragonimus Westermanii. — Endemic hemoptysis has thus 
far been confined to Japan, Formosa, and Corea, although cases 
have been reported from other eastern countries. On account 
of the frequency with which the Japanese are infected with this 
parasite it was named Distomum pulmonale and Distomum ringeri. 
Drs. Stiles and Hassall have recently recovered this parasite from 
the lungs of hogs raised in the United States. It has also been 
found in the lungs of cats and dogs, as well as in the lungs of 
certain wild animals. On account of the immigration of both 
Japanese and Chinese and of the temporary residence of United 
States troops in the tropics the spread of "parasitic hemoptysis" 
throughout America seems imminent. Dr. A. D. MacKenzie having 
recently reported a case from Portland, Oregon. 

Sputum. — The sputum is, as a rule, tinged with blood, and 
at irregular intervals attacks of hemoptysis occur which are 
usually induced by violent exercise. During these attacks the 
hemorrhage may be severe. In color the sputum may closely 
resemble that of lobar pneumonia. 

Detection. — Place a portion of the bloody sputum upon a 
slide, apply a cover-glass, and study under a one-fifth or one- 



436 THE SPUTUM. 

eighth objective. The pecuHar discoloration of the sputum will 
now be seen to depend upon the presence of numerous ova or their 
shells, as well as on the presence of red blood-corpuscles (Plate 29). 
The ova vary greatly in size and contour, although all will be 
found distinctly or imperfectly oval, presenting a smooth surface 
and a double outhne. They measure from ''80 to 100 [j. in length 
by 40 to 60 fi in breadth" (P. Manson). The parasite may be 
Cultivated in the laboratory by adding water to the sputum and 
keeping it at a moderate temperature for from four to six weeks. 
At the end of this time each mature ovum extrudes a cihated 
embryo. Pressure of the cover-glass upon the mature ovum may 
rupture the operculum, when the gyrated embryo escapes and 
may be seen swimming in the surrounding liquid. This parasite 
is reddish-brown, rather thick, oval in contour, and measures 
^'8 to 10 cm. in length by 4 to 6 cm. in breadth," and is covered 
with minute spines. 

Bilharzia. — There are numerous valid records of cases in 
which the ova of Schistosoma haematobium have been found in 
the sputum (see Urine, page 295). 

Amoeba Coli. — This parasite may be discovered m the sputum 
whenever an amebic abscess is evacuated through the bronchial 
tract, whether the abscess be pulmonary, hepatic, or subdia- 
phragmatic. I have observed a case in my private practice * 
in which the sputum contained many amebag over a period of 
four months. About two ounces of semigelatinous sputum were 
expectorated daily. It was often of a grayish color, streaked with 
blood, and contained numerous flocculi. Portions of this sputum 
appeared as though dotted with small droplets of dark-reddish 
fluid, and this characteristic persisted for weeks after the rupture 
of the abscess. Such sputum, when placed in a porcelain dish 
and allowed to stand, developed a. marginal, chocolate band; 
its tenacity was decided and its odor at times sweetish. Micro- 
scopically, motile amebae were studied under an oil-immersion ob- 
jective (Fig. 145), and occasionally an ameba was observed en- 
veloping a red blood-cell. Epithelial cells arranged in clusters 
and in radiating columns were also present. 

Trichomonades. — Trichomonades (Fig. 146) have been found 
in the sputum of pulmonary gangrene and in that from pus- 
cavities. The Balantidium coli (Fig. 147) may invade the respir- 
atory tract and consequently appear in the sputum. 

Whooping-cough. — Doechler and Kurloff claim to have ob- 
served the protozoon of whooping-cough in the sputum; yet, so 
far as I know, these observations have not received confirmation. 

*"Therap. Gaz.," April, 1902. 



PLATE 29. 







Paragonimus Westermanii. 
I. Six lung-flukes from hogs (natural size and color). 

^••F°,'^^/o^'; °^ a lung-fluke cyst, containing eggs of the lung-flukes (greatly 
magnified) (Stiles and Hassall). 



FUNGI, 



437 



Taenia Echinococcus. — Whenever cysts of this parasite rup- 
ture into the lung or the air-passages, both hooklets and scohces 
of the parasite may appear in the sputum; while less fre- 
quently small particles of the cyst membrane are expectorated. 
When these structures (Fig. 122) are found, the evidence points 
rather clearly to hydatid of the liver, yet hydatids of the lungs are 
not unknown. 

Ascarides. — This parasite or its ova is rarely found in the 
sputum (see Feces, page 414). 

Filaria. — The Hterature contains records of the Filaria san- 
guinis hominis having been found in the sputum. 






FUNGI. 

Among the non-pathogenic fungi that are known to appear in 
the sputum should be mentioned molds and yeasts, which are 
met with in the sputum of children and which may be seen 
in the salivary secretions of 
adults. Sarcinae are an occa- 
sional finding in the sputum 
of putrid bronchitis. Sar- 
cinae pulmonale are, as a 
rule, smaller than Sarcinae 
ventricuK (Fig. 138), but 
larger than'the sarcinae found 
in the urine. 

Pathogenic Fungi.— 
Actinomycosis of the respira- 
tory tract is distinguishable 
from other forms of pulmon- 
ary disease through the de- 
tection of small granules 

(Fig. 183) and thread-like particles (myceha) in the sputum (see 
page 301). 

Aspergillosis. — Aspergillus fumigatus has been found in 
the sputum of man by foreign observers, and was associated with 
pneurnomycosis. The aspergillus, when present in the sputum, 
is usually recognized by the detection of many thread-like particles 
(mycelia) (Plate 19). I have found Aspergillus fumigatus in the 
sputum of man but once, and in this instance there appeared to 
be no connection between the fungus and the disease from which 
the patient was suffering. It is not uncommon to find sputum 
secondarily infected with Aspergillus niger, and it is difiicult to 
distinguish microscopically between the mycelia of these two fungi. 





Fig. 183. — Actinomyces (after von Jaksch' 



438 THE SPUTUM. 

Dr. M. P: Ravenel has studied the Aspergillus fumigatus from the 
lung of a cow apparently suffering from pulmonary tuberculosis. 
The early writers regarded this organism as accountable for the 
destructive lesions of tuberculosis. 

Other fungi, as the Mucor corymbifer, are to be encountered 
in the sputum, and it should be further stated that many different 
molds may develop in the sputum after it has been exposed to 
the air of a warm room. As a rule, however, these fungi have no 
clinical significance, being commonly of extraneous origin. I have 
seen the yeast fungus in the sputum from tuberculous cavities. 

BACTERIA. 

Many bacterial species have been found in the sputum, and 
in a comparatively small number of instances a definite micro- 
organism will be found associated with a certain disease. I have 
never seen a specimen of sputum in which there was a pure in- 
fection with any one bacterium; but, on the other hand, the rule 
is to find a number of organisms in each sputum. Among the 
bacteria commonly encountered should be mentioned the pneumo- 
coccus, the streptococcus, the staphylococcus, a large diplococcus, 
the Bacillus typhosus, the Bacillus coh communis, Friedlander's 
bacillus, the Bacillus diphtheriae, the bacillus of influenza, the 
Bacillus tuberculosis, and the streptothrix. 

Microscopic Study of the Sputum. — Sputum should be col- 
lected in the manner described on page 426, and sent promptly to 
the laboratory. When the specimen is received, it should be 
poured into a clean glass dish in order to secure as large a surface 
as possible. Select from the sputum thus spread out any small 
caseous or bloody particles that may be apparent, place them upon 
a microscope slide, and then crush them and spread into a thin 
layer over the surface. It is my custom to hold the slide within the 
grasp of a slide forceps (Fig. 184, the author's device for this pur- 
pose) while the sputum is being smeared upon its surface. With- 
out removing the slide from the grasp of the forceps pass it three 
times through the flame of a Bunsen burner to fix the specimen. 

Tubercle Bacilli. — Staining. — i. Add a few drops of car- 
bolfuchsin to the specimen (5 per cent. carboHc acid, 90 parts; 
concentrated alcoholic solution of fuchsin, 10 parts), and hold 
it above the flame until the staining solution begins to steam. 

2. Wash in water, holding the forceps in such a manner that 
the stream strikes the slide near one end and then floods over the 
specimen. 

3. Without drying add to the specimen a few drops of Gab- 



BACTERIA. 439 

belt's methylene-blue solution (methylene-blue, 2 parts; solution 
of sulphuric acid (25 per cent.), 100 parts), and allow to stand 
for two minutes, when wash in water and dry over the flame. 

4. The specimen may now be mounted in Canada balsam and 
kept as a permanent specimen, in which case it is well to allow the 
balsam to harden before studying with an oil-immersion objective. 

In routine laboratory work it is my custom to apply the cedar 
oil directly to the specimen without the appHcation of a cover- 
glass. In searching for the diplococcus and organisms other than 



Fig. 184.— Author's combined slide and cover-glass forceps. Forceps in the act of picking the 

slide from the table. 




Fig. 185. — Forceps with the slide locked in position. 




Fig. 186.— As a cover-glass forceps. 

the tubercle bacillus equally satisfactory results are obtained by 
staining with a 2 per cent, aqueous solution of methylene-blue. 
Since tubercle bacilli are not uncommonly found in sputum from 
cases in which the general clinical features are far from suggestive 
of tuberculosis, it is a safe precaution to stain all sputa for the 
tubercle bacillus. I have repeatedly seen cases of large tubercular 
cavities in which it was impossible to stain the tubercle bacillus 
in the sputum by the above method. In three such cases studied 
at the Philadelphia Hospital I was privileged to witness autopsies, 



440 THE SPUTUM. 

during the course of which pus taken directly from the cavities 
showed many tubercle bacilli after this method of staining. 

Caution. — Whenever there are valid reasons for believing that 
tubercle bacilli are present in the sputum, the following treatment 
will materially facilitate their detection : 

Place the sputum in an ordinary vasehn bottle and tie over its 
mouth three or four thicknesses of gauze tightly — to prevent dust 
from entering the bottle. Set the specimen aside for several days 
and then examine for tubercle bacilli. The processes of decompo- 
sition appear to destroy certain substances (probably fats), which 
in the fresh sputum prevent the tubercle bacilH from taking the 
stain. A method which I have found most satisfactory for stain- 
ing such specimens is to smear the caseous particles of the sputum 
on slides and allow them to dry in the air. The specimen is then 
fixed either by passing it directly through the flame or by keeping 
it upon a hot stage (see Blood, page 74) for from twenty minutes 
to one-half hour. Specimens may also be fixed by immersing 
them in equal parts of absolute alcohol and ether. Specimens 
fixed by either of these methods should be immersed in a weak 
solution of fuchsin for from twelve to twenty-four hours (carbol- 
fuchsin, J dram; water, 2 ounces). 

By these methods it will frequently be found that tubercle 
bacilli are present in sputum in which it has been impossible to 
demonstrate them by the rapid method of staining previously 
described. This staining peculiarity of the tubercle bacillus is 
most commonly encountered early in tuberculosis, before the 
clinician is able to detect evidence of pulmonary involvement by 
the methods of physical diagnosis. 

Anilin-gentian-violet. — Gentian-violet forms a most satisfac- 
tory stain for the tubercle bacillus, and, while I am not prepared 
to state that it has advantages over carbolfuchsin, yet in my hands 
it has been found equally reliable. I began using this stain six 
years ago in the Philadelphia Hospital, and have found no cause 
for changing to any other. 

Sterling's Stain. — 

Gentian-violet lo gm. 

Anilin oil 4 " 

Alcohol (95 per cent) 20 " 

Distilled water 176 c.c. 

Add the anilin oil to the alcohol, and dissolve the gentian-violet in water. 
Add solution of gentian gradually, shaking vigorously after each addition; filter. 

(i) Sterling's solution should be added to the specimen in the 
manner outlined on page 438, and the slide should then be carried 
over the flame, and heated to streaming for from one-half to one 



BACTERIA. 



441 



minute. (2) Next wash in water to remove all excess of stain. (3) 
Then treat the specimen with a few drops of a 0.5 per cent, solu- 
tion of nitric acid until the specimen has apparently given up all its 
violet color. (4) Wash in water. (5) Counterstain with a few drops 
of a saturated alcohoHc solution of Bismarck-brown for from one- 
half minute to one minute. (6) Wash in water to remove all 
stain; dry between layers of filter-paper, and mount the specimen 
in Canada balsam. Under an oil-immersion objective the tubercle 
bacilli will be found to be stained a deep violet ; all other bacteria 
will be stained with the Bismarck-brown; the surrounding cells 
will be stained a light or mahogany brown; the nuclei of the 
epithehal cells and of the leukocytes will be stained somewhat 
darker than the protoplasm. 

Differentiation. — The tubercle bacillus is to be distinguished 
from the following organisms, all of which are acid-fast (do not 
decolorize readily by acids or by alcohol) — viz.. Bacillus lepra, 
smegma bacillus, the butter bacillus of Rabinowitch, and the grass 
bacillus. 

TABLE SETTING FORTH THE TINCTORIAL AND CULTURAL DIF- 
FERENCES OF "ACID-FAST" BACILLI WITH SPECIAL REFER- 
ENCE TO THE SOURCES FROM WHICH SUCH BACILLI ARE 
OBTAINED. 



Tubercle Bacillus. 

1. When stained with 

carbolfuchsin, 
does not give up 
its red color when 
counter stained 
for a long time 
with Gabbett's 
acid-blue solu- 
tion. 

2. Does not stain well 

with aqueous so- 
lutions of anilin 
dyes. 

3. Does not decolor- 

ize when treated 
with absolute al- 
cohol. 



Cultures develop 
only upon a spe- 
cial medium, and 
growth does not 
appear for from 
ten days to two 
weeks. 

Found in the spu- 
tum, saliva, nasal 
secretions, feces, 
exudates, transu- 
dates, tissues, and 
rarely in urine, 
blood, and in 
milk. 



Lepra Bacillus. 
. Retains its red 
color. 



2. Stains. 



Retains its red 
color, but is de- 
colorized in a 
shorter time than 
is the tubercle 
bacillus. 

Cultivation ques- 
tionable. 



Recovered from 
sloughing sur- 
faces, nasal dis- 
charge?^, in blood 
recovered by in- 
cising a leprous 
nodule and apply- 
ing firm pressure; 
and from the cir- 
culating blood. 



Smegma Bacillus. 
I. Retains its red 
color. 



Not readily stain- 
ed. 



3. Decolorized. 

Moeller states 
that the smegma 
bacillus is alco- 
hol-proof. 

4. Cultivated on spe- 

cial medium ques- 
tionable, and in 
this way differs 
from Bacillus tu- 
berculosis. 



Recovered from 
smegma of man 
and from that of 
the lower ani- 
mals ; also from 
the skin of the 
groin, axilla, and 
from the anus 
and the urine. It 
is rarely found 
in exudates, the 
tissues, and in 
sputum. 



Moeller's Grass 
Bacillus and the 
Butter Bacillus. 

I. Retains its red 
color. 



2. Not readily stain- 
ed. 



3. Not decolorized. 



4. Grows luxuriantly 

and with rapidity 
upon nearly all 
forms of culture- 
media when kept 
at both room and 
at incubating tem- 
peratures. 

5. Found about sta- 

bles, upon hay, 
and in milk, but- 
ter, the feces of 
cattle, and is to be 
always looked for 
in urine and feces 
of man. 



442 THE SPUTUM. 

Clinical Significance. — Tubercle bacilli, when found in 
the sputum, furnish conclusive evidence of the existence of a 
tuberculous lesion along the course of the respiratory tract. In 
the case of a small ulceration of the bronchus the number of tubercle 
bacilli present in the sputum may be very great; thus it is possible 
to find many tubercle bacilli in the sputum of persons who show 
no evidence of pulmonary involvement upon a physical examina- 
tion; and in this class of cases it is not infrequent to find the 
patient gaining in weight. Tuberculosis of the larynx is also 
likely to cause great numbers of tubercle bacilli in the sputum. 
It is the rule to find tubercle bacilli in the sputum of persons in 
whose lungs there exists an ulcerative process or a cavity of tubercu- 
lous origin. 

Characteristics of Tubercle Bacilli. — In the sputum of per- 
sons suffering from pulmonary tuberculosis of an acute and 
rapid nature the tubercle bacilli are, as a rule, short, and are less 
likely to show distinct cross-striations (segmentation) than are 
the bacilli recovered from the sputum of persons suffering from a 
chronic type of the disease. In the study of 600 specimens of 
sputum from nearly 400 different patients it was found that wher- 
ever the bacilli were short and failed to show segmentation, the 
course of the disease was at that time rapid. It was further 
found that upon sending such patients to the mountains larger 
segmented bacilli w^re found in their sputum whenever there was 
noted a decided amelioration of the symptoms; and that in the 
sputum of patients returning from the mountains apparently in 
perfect health large, segmented, and branching forms of bacilli 
were often detected. 

Other Bacilli. — Recent research has demonstrated that a 
number of bacilli that are not usually regarded as pathogenic for 
man also possess the property of retaining the red color from 
carbolfuchsin stain upon being treated with weak solutions of acids 
and with alcohol (see Differential Table, page 441). 

Other members of the acid-fast group of bacilli have been 
recovered from the sputum and in mucus from the respiratory 
passages. It appears possible that certain of the reports of tubercle 
bacilli having been detected in both the sputum and the urine 
are in error; I am, therefore, prompted to insist that a most impor- 
tant clinical feature here outlined is the differentiation between 
the tubercle bacillus and other acid-fast bacilli. Rosenberger has 
contributed an admirable monograph upon this subject. "^ 

Diphtheria. — During the course of diphtheria the sputum 
w^ll commonly be found to contain the diphtheria bacillus, which 

*"Proc. Path. Soc. Phila.," Dec. lo, 1903. 



PLATE 30. 




A. Sputum showing tubercle bacilli stained with carbolfuchsin and Gabbett's 
methylene-blue solution (obj. B. and L. one-twelfth oil-immersion). 

B. Sputum of anthracosis, showing particles of coal-dust stained with methyl- 
cne-blue (obj. Spencer one-twelfth oil-immersion). 



BACTERIA. 



443 



may be recognized by its characteristic staining and also by the 
result of cultures made directly from the fresh sputum. Culture 
studies of sputum, however, are not practical, and constitute a 
circuitous route to a diagnosis. 

Influenza. — The sputum in this disease may contain slender 
bacilli which stain readily by the ordinary anilin dyes. For their 
cultivation a special medium is necessary — Loffler's blood-serum 
will be found to serve well for this purpose, after the surface of 
the medium has been smeared with fresh blood, since the latter 
appears to provide certain substances necessary for the develop- 
ment of this organism. 

Acute Bronchitis. — Early in acute bronchitis the expectora- 
tion is small in amount, transparent, and contains but few cellular 
elements. When studied 
microscopically, many des- 
quamated epithelial cells 
are to be found which 
represent the various forms 
common to the bronchial 
tract. Many of these are 
originally ciliated, although 
it is rare to find ciliated 
epithelial cells in the 
sputum. Leukocytes are 
always present, though, as 
a rule, in small numbers; 
and red corpuscles may be 
found, varying in number 
with the degree of irrita- 
tion. 




~r , • , -I Fie. 187. — Bacillus of influenza, from a gelatin cul- 

-Later m tne course ture (X 1000) (Itzerottand Niemann). 



of acute bronchitis the spu- 
tum becomes more abundant, opaque, or turbid, and acquires 
a yellowish or greenish color, depending upon the number of 
leukocytes or pus-cells added. At this time the number of epi- 
thelial cells is found to be greatly lessened. 

Bacteriology. — Patton * suggests the terms "streptococcus 
bronchitis and staphylococcus bronchitis." The latter variety of 
infection is highly hable to chronicity; the sputum contains many 
staphylococci, which are often collected in such dense aggregations 
as to prevent their study with a high-power objective. 

In the case of streptococcic infection the sputum contains 
innumerable streptococci, and where this form of infection is mild, 
it is differentiated from the staphylococcic bronchitis through a 
microscopic study only. 

* "New York Med. Jour.," Mch. 28, 1903. 



444 THE SPUTUM. 

The bacteria common to the sahva are also present in the 
sputum of acute bronchitis, but seldom in sufficient numbers to 
attract special attention. 

Chronic Bronchitis. — It can scarcely be said that there is 
any sputum characteristic of this affection, since the expectorated 
material may vary within wide limits during the course of this 
disease. When the sputum is profuse and, as is sometimes the 
case, expectorated in mouthfuls, the term bronchorrhea is applied. 
The sputum is, as a rule, yellowish or yellowish-green in color, 
varying in shade with the number of pus-cells present and the 
degree or stage of their degeneration. 

Many micro-organisms are found in the sputum of chronic 
bronchitis, among which are to be mentioned streptococci, staphylo- 
cocci, both large and small bacilli, and bacilli in chains and 
bundles of chains. 

Pneumococcus. — The pneumococcus is a small diplococcus 
which occurs in the sputum from cases of lobar pneumonia, in 
which it is often the only organism present and always in great 
numbers. The diplococcus (Plate 31) is well stained by Gabbett's 
methylene-blue solution ; but its peculiar contour (biscuit forma- 
tion) is brought out more prominently by Bismarck-brown, so that 
when the specimen is carefully stained, each coccus is seen to be 
surrounded by a narrow hyaline space which is bounded by a faint 
marginal band (capsule). Encapsulated pneumococci are always 
to be seen with difficulty, and, while the majority of authors attach 
great importance to this finding, it is my experience that they are 
commonly met with in the sputum of healthy persons, and that 
they are only pathologic when present in the sputum in great 
numbers and in rather dense aggregations. The pneumococcus 
stains by Gram's method. 

Capsular Stain. — The capsule of this organism is rendered 
apparent by preparing and fixing the specimen as previously 
outlined. Next apply a i per cent, solution of acetic acid for from 
one to two minutes; remove the acid by washing and dry in the air. 
Then stain the specimen for from fifteen to forty seconds with 
a solution of anilin-gentian-violet, which is made as follows: 
Place in a test-tube one part of anilin oil and 20 parts of water; 
shake thoroughly; filter; preserve the filtrate in an amber-colored, 
glass-stoppered bottle. A saturated alcoholic solution of gentian- 
violet is now prepared, filtered, and the filtrate similarly preserved. 
These two solutions should be mixed a short time before use in 
the following proportions: 

Anilin-oil solution 9 parts 

Gentian-violet solution i part. 

Mix and filter. 



PLATE 31. 




A. Sputum containing plague bacilli and diplococci, stained with an aqueous 
solution of methylene-blue (obj. B. and L. one-twelfth oil-immersion). 

B. Sputum showing pneumococci. 




C. Scraping from tonsil stained with L5flEler's methylene-blue, showing diph- 
theria baciUi, diplococci, and streptococci (obj. Spencer one-twelfth oil-immersion). 



BACTERIA. 445 

Bacillus of Friedlander. — The pneumobacillus appears in 
great numbers in the sputum of persons suffering from lobar 
pneumonia whenever the disease is due to this parasite (Fig. i88). 
It stains readily by the same methods as does the pneumococcus, 
showing also a capsule formation. Friedlander's bacillus may 
enter the blood, and is to be found in the pus from abscesses 
and from inflamed joints complicating an attack of Friedlander's 
pneumonia or developing as sequelae of this disease. 

A number of micro-organisms are usually present in such 
sputum; the longer the sputum is retained in the bronchi, the 
more numerous are the bacteria. A few red blood-cells may 
be found, and epithehal cells are also present, although, as a 
rule, less plentiful than in the early stage of acute bronchitis. 
Epithelial cells, showing evidence of fatty and of myeloid de- 
generation, are also met with and are 
probably derived from the alveoli of the ^ . 

Bronchopneumonia. — Bronchopneu- ^^S 
monia is not placarded by a characteristic , \v "' . ■ 

sputum. The sputum may contain differ- / *" { / 

ent bacteria, among which are the pneumo- -, 
coccus, Streptococcus pyogenes, Staphylo- ' x., 

coccus pyogenes, bacillus of Friedlander, 

Bacillus pyocyaneus, diphtheria bacillus, baciiiu^'inp\^fromJfu"mJn- 
Bacillus typhosus. Micrococcus tetragenus, one-tweTftr). ^°^^- ^^""'^" 
and meningococcus. It is the rule to find 

more than one bacterium present in the sputum of catarrhal 
pneumonia. 

Bronchial Asthma. — At the beginning of an attack of asthma 
the sputum is scanty, and may be clear, grayish, or rarely red, owing 
to the presence of red blood-cells. It is always frothy. Asthmatic 
sputum is usually characterized by the presence of small, yellowish 
or grayish particles, "bronchial spirals" (see Spirals, page 433), 
Charcot-Leyden crystals (Fig. 189), and leukocytes. Many of the 
leukocytes show a special affinity for basic dyes, while the majority 
of them are decidedly eosinophilic (Fig. 190). 

PAilmonary Abscess. — The fresh sputum from an abscess 
of the lung does not emit a decided odor. When subjected to 
microscopic study, it will be found to consist principally of pus- 
cells, hematoidin crystals, fragments of lung tissue, and numerous 
crystals, among which cholesterin and those of the fatty acids arc 
most common. Fibers of elastic tissue are not unusual findings 
in the sputum of abscess (see Elastic Tissue, page 434). Hepatic 
and other forms of amebic abscesses have been discussed under 
Animal Parasites (Amoeba, page 388). 



446 THE SPUTUM. 

Pulmonary Gangrene and Putrid Bronchitis. — In these 




Fig. 189. — Charcot-Leyden's asthma-crystals (after Riegel). 

conditions the sputum presents practically the same characteris- 
tics, so that it is scarcely practicable to make a differential diagnosis 

from the microscopic examin- 
ation of the sputum. They 
are distinguished one from 
another by microscopic study 
only, by the finding of par- 
ticles of pulmonary tissue 
derived from the parenchyma 
of the lungs in the case of 
gangrene. The sputum of 
gangrene deposits a rather 
characteristic sediment when 
placed in a conic glass and 
allowed to stand for several 
hours. At the end of that 
time it will be found to have 
separated into strata: the 
inferior stratum is grayish- 
yellow or brown and con- 
tains pus, small particles of 
a brown or greenish tint which vary in size from that of a 
millet-seed to that of a kernel of corn, and, less often, particles 




Fig. 190.— Sputum from a case of asthma, 
showing leukocytes, some containing eosino- 
phile granules ; free eosinophile granules ; and 
micrococci ; stained with eosin and methylene- 
blue (Jakob). 



BACTERIA. 447 

of lung tissue. On microscopic examination this sediment 
will be found to contain triple phosphate crystals, leucin and 
tyrosin, hematoidin, and, at times, other crystals of a question- 
able nature. Pus-cells and leukocytes are plentiful, and the 
masses detected by the naked eye are found to be composed 
principally of pigment. Elastic fibers, oil-droplets, crystals of the 
fatty acids, and bacteria are among the usual findings. The 
Leptothrix pulmonalis (Fig. 193) deserves special mention. It is 
recognized, in addition to its chain-like formation, by the fact that 
it is colored violet or blue by Lugol's solution. The detection 
of elastic fibers (alveolar arrangement. Fig. 182) serves as the only 
positive differential point between putrid bronchitis and pulmo- 
nary gangrene; but in my own experience this tissue is seldom 
found in the latter condition, of which it is said to be charac- 
teristic. 

The middle stratum is transparent, and in it are suspended 
particles of mucus; while the superior stratum is usually of a dirty- 
yellow color and is covered with a decided froth. 

Pulmonary Tuberculosis. — The sputum from a case of 
pulmonary tuberculosis displays nothing characteristic, although 
when complications exist, the sputum may be placarded by certain 
peculiarities. 

Incipient Phthisis. — Here the sputum is usually scanty, 
grayish-yellow or whitish in color, frothy, and tenacious. The 
bulk of the day's product is ejected in the morning, and even this 
may not exceed a few cubic centimeters. Hand in hand with the 
progressing pulmonary involvement the sputum will be found to 
increase in quantity. After cavity formation the sputum displays 
coin-like masses of yellowish or grayish mucopus (see Nummular 
Sputum, page 431). 

Microscopically the tubercle bacillus is to be detected (see 
page 438), but red cells are not usual, and in other respects the 
sputum of tuberculosis is practically the same as that of chronic 
bronchitis. 

When the admixture of blood is large, the entire sputum may 
form a rather dense clot; but at other times the presence of a 
small quantity of blood controls the color of the sputum. Dark 
and blackish sputum is occasionally seen (see Color, page 430) > 
and, in cases in which the hemorrhage is very large, it is often 
difficult to determine whether the blood is of pulmonary, gastric, 
pharyngeal, or aneurysmal origin. In this connection I am 
prompted to offer the following differential table: 



448 THE SPUTUM. 

Pulmonary Hemorrhage. Gastric Hemorrhage. 

1. Evidence of preexisting pulmonary i. Referable to the throat, stomachy 

disease. liver, or heart. 

2. Preceded by thoracic oppressions 2. Preceded by giddiness, faintness, 

and a saline taste. and nausea. 

3. Blood ejected by coughing when 3. Blood ejected by vomiting or by 

hemorrhage is small. clearing of the throat. 

4. In profuse hemorrhage and when 4. Blood of gastric origin dark, as a 

ejected immediately blood arterial rule; blood of pharyngeal origin, 

in color. bright red. 

5. Alkaline reaction. 5. Gastric blood acid, pharyngeal 

blood alkaline, in reaction. 

6. Blood mixed with particles of muco- 6. May contain undigested food. 

pus. 

7. A pronounced beaded froth. 7. Froth less marked. 

8. Microscopically tubercle bacilli and 8. Microscopically, Sarcinae ventriculi, 

elastic fibers. starch-granules, particles of food, 

and, in the case of carcinoma, 
large bacilli (Oppler-Boas, page 
350), and rarely carcinoma cells. 

The color of the sputum may be so modified by retention of the 
blood in an edematous lung that it is unrehable as a distinctive 
feature between gastric and pulmonary hemorrhages. In such 
cases either form of hemorrhage may result from cardiac in- 
sufhciency. 

Edema of the Lung. — The sputum associated with this 
condition is always profuse, watery, and presents a heavy froth. 
In color it will be found to vary from a translucent fluid to that of a 
dirty reddish or brown liquid. The darkening results from the 
admixture of blood-cells and the presence of methemoglobin. 
On account of the fact that such sputum is the result of transudates 
it is found to be rich in serum-albumin; while microscopically it 
contains red and white blood-cells in variable numbers; although 
the red cells are apparently too few to account for the decided 
color which is often present. 

Pneumonia. — The characteristic sputum of this disease is to 
be seen during the early stage of consolidation in lobar pneumonia, 
at which time it is scanty and tinged with blood (rusty). Such 
sputum is highly tenacious, and shows no tendency to flow from 
the side of the receptacle (see Tenacity ^ page 429). In this stage 
of the disease the microscope shows the presence of red corpus- 
cles, upon which the rusty color may depend; but in certain in- 
stances very few red cells are present, and then the color depends 
upon the presence of hemoglobin which has been separated from 
the corpuscles. A varying number of leukocytes is always present, 
and upon staining, many of these cells are seen to be eosinophilic, 
a condition more common in the sputum of bronchial asthma 
(page 445). Alveolar epithehal cells are, as a rule, present, and 



BACTERIA. 449 

many of these are studded with granules of pigment, oil-globules 
(fat), and myehn areas. Larger epithelial cells may be seen, 
which are probably derived from the larger bronchial tubes or 
from the mouth. Fibrinous casts may be detected by the naked 
eye (see Fibrinous Casts, page 432), and, in the event of such 
complications as pulmonary abscess or gangrene, the sputum will 
present the characteristics of these conditions (see Abscess, Gan- 
grene). 

Pneumococcus. — The pneumococcus (described on page 444), 
which is present in great numbers during the course of this dis- 
ease, and particularly in the early stage of hepatization, will be 
found massed together in rather dense aggregations throughout the 
field. From this arrangement, unless an oil-immersion objective 
is employed, the organisms are likely to be mistaken for staphy- 
lococci. After resolution has begun (third stage), the sputum of 
pneumonia cannot be said to be characteristic, but simulates that 
of a catarrhal bronchitis. 

Organic Heart Disease. — In cases of organic heart disease 
it is not uncommon to find blood-stained sputum : but such sputum 
may be readily distinguished from the sputum of pneumonia, 
since it will be found to contain but few diplococci. Alveolar 
epithelial cells in the bodies of which small brownish or brown- 
ish-red granules of hematoidin are deposited — "heart-disease 
cells" — are a rare finding. In the event of a hemorrhagic infarct 
having occurred in the lung, the sputum is at first red in color, 
iDut later becomes dark and resembles the condition seen when 
blood is retained in the bronchi before it is ejected. 

Pneumoconiosis. — Under this caption it has been deemed of 
value to describe briefly the sputum seen in cases of anthracosis, 
chalicosis, stycosis, and siderosis. 

Anthracosis. — This condition is rather common in coal- 
miners and in persons residing in a district in which particles of 
coal-dust and carbon are constantly floating in the air. Early 
during this condition, when the lung tissue has not become seri- 
ously embarrassed by the deposit of such dust, the sputum is 
slight in amount, and probably the only expectoration of the 
day occurs upon rising or after a meal. Later, w^hen a decided 
bronchitis is present as the result of the foreign material in the 
mucous membrane of the finer bronchi, the sputum becomes more 
copious and may, at times, contain large mucopurulent granules, 
spirals, and rarely fibrinous casts. At times during the course of 
anthracosis the sputum will present to the naked eye a variable 
degree of browning or an irregular distribution of black pigment. 
Such sputum should be stained for the tubercle bacillus. It has 
29 



45° 



THE SPUTUM. 



been my privilege to detect this organism in more than one hun- 
dred specimens of anthracotic sputum. The characteristic find- 
ing, however, is that of small particles of coal-dust, which are 
readily detected under a one-fifth objective; and when viewed 
under an oil-immersion objective, these masses cannot be mis- 
taken (Plate 30). The other microscopic findings are those 
common to chronic bronchitis and to asthma. 

It is not uncommon to detect particles of carbon in the sputum 
of persons who smoke to excess; but these particles dift'er from 
those present in the sputum of coal-miners by the facts that they 
are grayish or broAvnish in color, and that they do not present clear- 
cut surfaces, a characteristic feature of the particles of coal-dust 
seen in anthracotic sputum. 

Chalicosis. — Chalicosis is a condition in which the sputum 
contains small particles of the sificates. 

Stycosis. — Stycosis is a condition in which the sputum is seen 
to contain particles of lime, plaster-of-Paris, etc. The condition 
has been described at length by A. Robin. Like anthracosis, 
stycosis is accompanied by cough and free expectoration. 
Stonemason' s lung results from the inhalation of lime-dust and 
particles of stone, the presence of which may be detected in the 
sputum by its chemic reaction. Particles of hme are also to be 
found within the alveolar epithelium and in the leukocytes. 
Other characteristics of the sputum are practically those of chronic 
bronchitis. 

Siderosis. — The sputum in cases of siderosis is, as a rule, 
brown or black in color, while in other respects it resembles that 
of chronic bronchitis. ^Microscopically many alveolar epithelial 
cells and leukocytes are to be seen, both of w^hich are often studded 
with a variable amount of reddish pigment. Sputum containing 
iron, Avhen treated with ammonium sulphid, develops a black color, 
due to the formation of iron sulphid. To another portion of a 
highly colored sputum supposed to contain iron add hydrochloric 
acid and potassium ferrocyanid; the presence of iron is indicated 
by the development of a Prussian-blue color. 



CHEMIC STUDY OF THE SPUTUM. 

ORGANIC SUBSTANCES. 

The sputum will be found to contain certain organic substances 
other than those previously described, among which albumins, 
ferments, glycogen, and volatile fats deserve brief mention. 



ORGANIC SUBSTANCES. 451 

Proteids. — Among the proteids commonly found in the sputum 
serum-albumin, a liberal quantity of mucin, and nuclein are 
normal constituents. In the expectoration from cases of croupous 
pneumonia, purulent bronchitis, abscess, draining through the 
bronchial tract, and cases in which pus-cells have gained access 
into the sputum peptones will be found as a constant constituent. 

Detection. — Serum-albumin is best detected as follows: 
treat the sputum with dilute acetic acid, filter, and test the filtrate 
as described under the Chapter on Urine (page 206). 

Excess. — A large amount of serum-albumin will be found 
in the sputum of pulmonary edema, and in allied conditions in 
which the albuminous constituents of the blood are ejected with 
the sputum. 

Ferments. — In pulmonary gangrene and in putrid bronchitis 
the sputum has been found by Stolnikow to contain a ferment 
which, in certain respects, resembles the pancreatic ferments. It 
is insoluble in glycerin, and may, therefore, be extracted from the 
sputum by the aid of this substance. This ferment, when present 
in the sputum, is probably suggestive of a highly destructive 
process ifi the lung. 

Glycogen. — Glycogen may be present in the sputum, and its 
detection is accomplished by the methods suggested by Williamson 
(see Blood, page 68). 

Fatty Acids. — In order to obtain the volatile fatty acids present 
in the sputum dilute with water, acidify wdth phosphoric acid, and 
distil. Examine the distillate for the presence of volatile fatty 
acids according to the technic described in the chapter on Feces. 
Acetic, butyric, and carbonic acids are occasionally found. The 
non- volatile fatty acids of the sputum are detected by first acidify- 
ing the sputum with phosphoric acid and extracting with ether. 
Repeatedly shake this ethereal extract with an aqueous solution 
of sodium carbonate; by this means the acids are converted into 
their respective salts, but remain suspended in the solution. Re- 
move the ether by siphoning, and obtain the fats after the ether 
has been evaporated. Indol, phenol, and skatol appear in the 
sputum of pulmonary gangrene. 



CHAPTER VI. 
BUCCAL SECRETION. 

The salivary secretion is properly classed among the mixed 
secretions, since it is derived in part from the salivary glands 
(parotid, submaxillary, and sublingual) and in part from the ducts 
of the mucous glands within the mouth, all of which open into the 
buccal cavity. The saliva is subject to great chemic variations, 
since the disproportionate function of any one set of these glands 
or all of them materially alters its chemic composition. 

Collection. — Direct the patient to wash the mouth, brushing 
the teeth carefully with a solution of sodium bicarbonate, and 
afterward rinsing the mouth thoroughly with cold water. Touch 
the inner surface of the cheek or the edge of the tongue with a 
glass rod that has been dipped into dilute acetic acid or dilute 
hydrochloric acid. As soon as the acid touches the mucous mem- 
brane the saliva will be seen pouring into the buccal cavity from 
a number of points. The patient may be allowed to expectorate 
the saliva directly into an earthen receptacle, or the secretion may 
be siphoned into a convenient receptacle as follows: A glass tube 
may be arranged with a bulbous expansion at one end through 
which there are many small openings. This portion of the tube 
is placed beneath the tongue, while the remainder of the tube, 
bent at a proper angle, empties into the receptacle. 

PHYSICAL PROPERTIES. 

Normal fresh saliva is colorless or may present a slight bluish 
hue; it usually is fluid in consistence, though at times semifluid, 
tenacious, and stringy. Upon standing in a conic glass the saHva 
separates into two layers: an inferior cloudy or turbid stratum, 
which contains the majority of the morphologic elements, and a 
superior stratum, usually the deeper and clearer, which is often 
covered with a beaded froth. 

Quantity. — The quantity of saHva secreted a day will be found 
to vary between 200 and 1500 gm. (6 to 48 fl. oz.). 

Reaction and Specific Gravity. — Normal saHva is alkahne 
in reaction and has a specific gravity of from 1.002 to 1.006. 

452 



CHEMISTRY. 453 



CHEMISTRY. 



On account of the disproportionate activity of the different 
glands it is with difificuhy that any cHnical observations of value 
can be made in this direction, except in the saliva of a few special 
conditions (ptyaHsm and opium-poisoning). Traces of albumin, 
mucin, and, less often, potassium salts are to be found in this 
secretion. In addition, a ferment, capable of changing starch into 
sugar, and other salts are normally present. When it is possible 
to obtain the secretion of the parotid gland, such sahva has been 
found to contain carbonic acid, nitrogen, and oxygen. In health 
the buccal secretion concerns us, as clinicians, but little. During 
diseased states this secretion is diminished to such an extent that 
its study is impracticable, except in cases of ptyalism, in which 
the secretion is profuse. For chemic analysis it is possible to 
collect pure saliva, but this is best approximated by directing the 
patient to rinse the mouth carefully after each meal and to ex- 
pectorate all secretions that accumulate in the mouth into a clean 
vessel. In this way the twenty-four-hour product may be col- 
lected, and its specific gravity, reaction, consistence, etc., ascer- 
tained after the manner described for the study of urine. 

Sulphocyanids. — Place a few cubic centimeters of saliva in 
a test-tube and treat with a solution of ferric chlorid. When sul- 
phocyanids are present, a bright-red color develops which is 
unaffected by the application of heat or by the addition of acids. 
Should no red color appear, place 50 to 100 c.c. of sahva in a 
casserole and evaporate over a water-bath to a few cubic centi- 
meters. Repeat the test as above outlined. Sulphocyanids also 
give an emerald-green color when treated with cupric sulphate; 
precipitate the sahva with alcohol, filter, evaporate the filtrate 
to dryness over a water-bath, and to this residue add a few cubic 
centimeters of water. 

Opium Poisoning. — The saliva of persons poisoned with 
opium will give a cherry-red color when treated with ferric chlorid. 
This reaction depends upon the presence of meconic acid, and the 
color is not altered upon the addition of mercuric chlorid. The 
reaction (red color) due to sulphocyanids will be found to disappear 
when mercuric chlorid is added. 

Sugar. — Sugar may also be obtained from the saliva after the 
manner described in the Chapter on Urine (page 224), observing 
the above precautions, 

Diastatic Ferment. — The presence of a diastatic ferment may 
be detected as follows: Mix 5 c.c. of saliva with 50 c.c. of starch 
water, heat over a water-bath at a temperature of 40° C. (104^ F.) 



454 BUCCAL SECRETION. 

for one hour, at which time this mixture will be found to give 
definite reactions for grape-sugar should an amylolytic ferment be 
present. 

Control. — The mixed saHva should be tested for sugar before 
the process of heating is begun. 

Nitrites. — Nitrites of the saliva are demonstrated by adding 
a mixture of starch paste, dilute sulphuric acid, and potassium 
iodid. In the presence of nitrites an intense blue color develops. 

Greiss' Test. — Dilute a quantity of sahva with five times 
its volume of water, add a few drops of sulphuric acid and meta- 
diamidobenzol, and heat to 63° or 65° C. (145.4° to 149° F.). 
An intense yellow color is indicative of nitrites. 

MICROSCOPIC APPEARANCE. 

When examined under the microscope the saliva will be seen 
to contain a number of morphologic elements which are found to 
vary greatly both in health and in disease. 

The sahvary corpuscles are bodies which resemble the white 
blood-cells in many respects, but which dift'er from these bodies 
in the following particulars: they are larger; their protoplasm is 
usually more granular, and they do not possess the clear-cut 
margin so characteristic of the leukocyte. Red blood-cells may be 
found in pathologic saliva in connection with a variable number 
of leukocytes. 

Epithelium. — Epithelial ceUs are found in both pathologic 
and normal saliva. Since these cells are derived, as a rule, from 
the mucous membrane of the mouth and tongue, they vary greatly 
in number in health, and a variety of forms and sizes are always 
present. The morphologic characters, however, are governed by 
the respective layer of the mucous membrane from which the cells 
are derived. There is nothing characteristic of the epithelium 
ejected with the saliva, and when stained, they may show areas 
of degeneration; both the cell-bodies and the nuclei often stain 
abnormally. 

Bacteriology. — Molds are not a common finding in the buccal 
secretion. Fission-fungi are occasionally met with in healthy 
saliva, occurring in dense aggregations in various portions of the 
microscopic field. They are stained reddish with a solution of 
iodin and potassium iodid. The ray-fungus may be found in the 
saliva in cases of actinomycosis (page 458), and the thrush fungus 
is also an occasional finding (page 457). In one case in which 
favus involved the tonsils I recovered the fungus from the saliva 
(Fig. 192). 



BUCCAL SECRETION IN DISEASE. 



455 



The saliva may contain the bacteria of an infectious disease 
during an attack of that disease; for example, pneumonia and 
typhoid fever. Among other organisms found in the saliva de- 
serving special mention are : Leptothrix buccalis, Spiroch^ta den- 
tium, Vibrio buccalis, micrococcus of septic sputum. Micrococcus 
tetragenus, a bacillus found in connection with decaying teeth, 
Staphylococcus pyogenes albus, Staphylococcus pyogenes aureus, 
Streptococcus pyogenes, tubercle bacillus. Bacillus diphtheria. 
Bacillus pestis. Bacillus lepra, the fusiform bacillus, the spirillum 
of \'incent, the pneumococcus, a large diplococcus, meningococcus, 
and the diplococcus of Class (scarlatina). It is not infrequent to 
find bacilh in the saliva of healthy persons which in morphologic 
and cultural characteristics resemble closely the bacillus of diph-^ 
theria. In fact, at times it is impossible to distinguish between 
this pseudodiphtheria bacillus and the true Klebs-Loffler bacillus, 
except by the aid of inoculations. Cukures from the saliva are 
seldom of practical value; but when such studies are undertaken, 
the inoculation should be made from material obtained directly 
from the mucous surface of the buccal cavity. 



BUCCAL SECRETION IN DISEASE. 

For clinical significance of buccal secretion in disease, see p. 

534. 

Catarrhal Stomatitis. — Catarrhal stomatitis is a condition 
which is characterized by an increased quantity of saliva which 
is acid in reaction. Microscopically many epithelial cells, leuko- 
cytes, and, at times, red blood-cells may be found in the fluid. 

Should the condition progress to ulceration, the saliva becomes 
fetid, brown or blackish in color, and alkaline in reaction. At 
this stage of the disease the miicroscope shows many red blood- 
cells, leukocytes, tissue debris, and, at times, many fungi and 
bacteria. 

Ulcerative Stomatitis with Angina. — Of late the records of 
a number of cases of ulcerative stomatitis with angina have ap- 
peared in the literature. In this disease the saliva was found to 
contain the "fusiform bacillus and spirillum of Vincent." The 
majority of these reports have appeared in foreign periodicals, 
principally those of France and Germany; while the English 
literature shows few such records. Among the last should be 
mentioned the researches of Emil Mayer;* also a report of two 
cases by Fisher.f Vincent J first called attention to the fact that 
in certain forms of ulcerative angina fusiform bacilli and spirilla 
were to be found in the saliva. In 1897 the same author reported 

* "Amer. Jour. Med. Sci./' Feb., 1003. f Ibid., Sept., 1903. 

J "Annal. de I'lnstitut Pasteur," iSg6. 



45^ 



BUCCAL SECRETION. 



the studies of 14 additional cases in which these organisms were 
found.* In 1897 Bernheim pubUshed his findings in 30 cases of 
stomatitis with angina, although he did not regard the bacillus 
of Vincent as the etiologic factor in his cases. Niclot and Marotte 
have made an exhaustive bacteriologic study of the saliva in this 
condition, and from their conclusions I have made the following 
abstract, which embraces the characteristics of these organisms. 

Bacillus. — The fusiform bacillus (Fig. 191) is expanded at its 
center and displays pointed extremities; it is, as a rule, straight, 
but at times is slightly curved or bent upon itself. It measures 6 
to 12 [1 in length. In the smeared saliva it often appears in 
rather dense aggregations, sometimes resembling diplococci, and 

at other times resting at right 
angles to each other. The 
organisms are shghtly motile. 
They stain readily with the 
ordinary basic dyes; but, 
as a rule, they are nearly 
all decolorized by Gram's 
method, and those organ- 
isms which resist the decol- 
orizing process are usually 
involution forms, and are 
often found to show vacuola- 
tion and granulation. Spore- 
formation has not been de- 
termined. 

Spirillum. — The spirillum 
(Fig. 191) varies in its di- 
mensions, but is, as a rule, 
long and of uniform diameter throughout. It occurs singly or in 
clusters, and less often in dense masses. It is motile, and the 
motihty may persist for some hours, although it diminishes upon 
exposure to the air or at a low temperature. This organism is 
stained by the ordinary basic dyes, but is readily decolorized by 
Gram's method. In deep ulcerations both bacilli and spirilla 
are present, but where the ulcerative process is superficial, only 
fusiform bacilli are found. This rule, however, does not always 
hold true. Vincent's bacillus and spirillum may be found asso- 
ciated with the streptococcus, the pneumococcus, the Klebs- 
LofHer bacillus, and the colon bacillus in the secretion from 
superficial ulcerations, but should the secretion be taken from a 
deeper source, it is most likely to show only bacilli and spirilla. 

* "Bui. et Mem. Soc. Med. des Hop.," Mch., 1898. 




Fig-. 191. — Bacillus and spirillum of Vincent, 
from ulcer in case of ulcerative stomatitis. 
Stained by carbolfuchsin (obj. B. and L. one- 
twelfth oil-immersion ; X 1000 ). 



BUCCAL SECRETION IN DISEASE. 



457 



Thus far cultivation and inoculation have given negative 
results. 

Gonorrheal Stomatitis. — In a few instances stomatitis has 
been found to result from infection with the gonococcus, and 
while chancroidal infection of the mouth is occasionally seen, both 
these conditions must be extremely uncommon in America. In 
several cases of stomatitis, supposedly gonorrheal, I found, by 
cultural methods, that the organism in question was not the 
gonococcus, but an intracellular diplococcus which did not stain 
by Gram's method. 

Thrush. — Thrush is not an uncommon finding in the buccal 
secretions of children, while occasionally it may be encountered 
in the saliva of adults. In the latter case it is found in persons 
whose vitality is greatly 
reduced — e- g-, those 
suffering from tubercu- 
losis. In this disease 
the saliva is often acid 
in reaction, although 
the thrush fungus 
(Oidium albicans) may 
develop in an alkaline 
medium, yet it, like 
other fungi, will be 
found to develop well 
in acid media. 

D et ection. — Re- 
move a small portion 
of the white patch 
which appears on the 
mucous membrane, 
smear thinly upon a 
slide, and examine 

under a two-thirds or one-sixth objective, when the mycelia and 
the spores of this fungus will be readily detected (Fig. 192). 
Leukocytes, tissue debris, red cells, and branching, ribbon- 
like segments of the fungus are constant findings. Well- 
defined oval cells displaying one or more nuclei are also present, 
and the desquamated epithelial cells are commonly found in 
clusters of four to ten each. Later in the course of the disease 
the initial patches may coalesce, but this does not influence 
materially the characteristic features of the fungus. The mycelial 
threads of the thrush fungus arc well stained by anilin-gentian- 
violet and by an aqueous solution of methylene-blue. Staining 




Fig. 192. — Thrush fungus, epithelial cells, and leuko- 
cytes from a child suffering from ulcerative stomatitis 
(obj. Spencer one-sixth). 



45^ BUCCAL SECRETION. 

shows that each segment of the ribbon-hke bodies contains a 
highly refractive, especiaUy well-stained, portion imbedded near 
one extremity. These bodies (spores?) may be situated at each 
extremity of the segment; they are at times finely granular and 
oval in outline. Staining is by no means necessary for the study 
of this fungus, and satisfactory results are to be obtained by 
adding glycerin to the exudate and studying as previously outhned. 
Actinomycosis. — Pus containing the actinomyces is at times 
discharged with the buccal secretion. J. Wright reports a case of 
infection of the tonsil.* 

COATING OF THE TONGUE. 

The coating of the tongue when subjected to a microscopic 
examination may, in certain febrile conditions, contain great num- 
bers of various forms of epithelial cells, and dark cellular bodies, 
doubtless degenerated epithehum. Black coating is probably 
dependent upon a formation of pigmented papillas, while a white 
coating is normal for children and w^ill be found to accompany 
gastro-intestinal conditions in the adult. In these conditions 
epithelium, salivary corpuscles, and a few fungi miay be present. 

TARTAR OF THE TEETH. 

Chemically, the tartar on the teeth is composed of calcium 
salts; but, as a rule, it is found to be principally composed of 
calcium salts because of the greater solubility of the potassium 
and sodium salts. Either potassium or calcium may exist as 
urates, and in certain instances sodium urate forms the principal 
ingredient of the so-called tartar and scales. The above deductions 
are taken from a series of analyses made by Dr. James C. Attix. 

The urates preponderate in the tartar collected from the teeth 
of persons known to be of a rheumatic or uric-acid diathesis. 

Theory. — The secretions of the parotid, subhngual, and sub- 
maxillary glands are known to be rich in mucin, and contain CO 2 
prior to being poured into the oral cavity, when these secretions 
are under slight pressure. Upon escaping into the mouth this 
pressure is released, CO 3 escapes, and thereupon the precipitation 
of the contained salts is favored. This action is enhanced further 
in the presence of the lactic-acid fermentation. A shght acid 
reaction of the secretions of the mouth favors this process, because 
mucin is thereby made thick and viscid, thus entanghng the 
minute particles which go to make up these concretions. 

* "Amer. Jour. Med. Sciences," July, 1904, p. 74. 



TONSILLAR MEMBRANE. 459 

Characteristics. — These tartars are, as a rule, quite solid and 
granular. When the urates predominate in them, they have a 
yellowish hue, although they may at times be stained from the 
use of tobacco, etc. The color and consistence of the tartar de- 
posited upon the teeth of those suffering from a general peri- 
cementitis, as is seen in marked anemias, are variable: at times, 
light, and at other times dark; always offensive in odor and rich 
in particles of food and in lactic acid. 

Bacteriology. — Tartar from the teeth smeared out thinly 
upon a slide, when stained with carbolfuchsin or methylene-blue, 
will be found composed principally of long bacilli arranged in 
chains, and these chains in ribbon-like bundles (Leptothrix buc- 
calis). These organisms are stained a bluish red by a solution of 
iodin and potassium iodid. It has been at times regarded as a 
cause of dental caries, but many authorities claim that other 
organisms contribute largely toward this process. Streptococci 
and staphylococci are also to be obtained from the tartar collected 
about the teeth, but these organisms are not usually pathogenic. 

Pernicious Anemia. — Of recent years considerable attention 
has been given to the subject of dental caries, the tartar of the 
teeth, and the existence of a high grade of anemia. In fourteen 
cases of pernicious anemia in which the blood counts gave the 
number of red cells below 1,250,000 per cubic millimeter I found 
that the teeth were in bad condition in many, so that I was often 
able to recover pathogenic bacteria, cocci, and bacilli from this 
source. Again, in a rather large percentage of my cases, the teeth 
were found to be in perfect condition, and out of three cases 
studied through the courtesy of Dr. L. Webster Fox, two showed 
that the teeth had never required the attention of the dentist 
and were in perfect condition, while the third showed the teeth 
to be in a healthy state. 



TONSILLAR MEMBRANE, 

During the course of tonsillitis a membrane may be removed 
from the tonsil. When stained, this membrane is often found to 
contain streptococci, diplococci, staphylococci, or a combination 
of all in conjunction with bacilli. In scarlet fever Class claims to 
have found a large diplococcus in a high percentage of his cases. 
In catarrhal tonsillitis the secretions are liable to show many 
bacteria. 

Diphtheria. — In cases of suspected diphtheria it is often 
possible to diagnose the disease from a microscopic study of the 



460 BUCCAL SECRETION. 

false membrane. It is my practice to secure a small portion of the 
membrane by means of a forceps, and to smear it thinly upon a 
shde. The specimen is then fixed by heat, stained for three 
minutes with Loffler's methylene-blue solution, washed in water, 
dried, and studied under an oil-immersion objective. In the vast 
majority of instances it will be possible to detect typical diphtheria 
baciJIi in such secretions. I have employed this method and 
have at the same time mxade cultures as control tests and examined 
them after they had been kept for twenty-four hours in the incu- 
bator. In more than 70 per cent, of the cases it was possible 
to recognize the diphtheria bacihus beyond question of a doubt 
in the stained specimen, and in every instance these findings were 
confirmed by cultural studies. 

Caution. — It will often be found that the false membrane 
removed from the tonsil contains only streptococci, and rarely 
it will be found to contain bacilli. Still the bleeding surface which 
results from the removal of such a membrane appears to the naked 
eye identical with that of diphtheria. Again, the membrane may 
not leave a bleeding surface after removal, and yet the microscope 
will show Klebs-Loffler bacilli in great numbers. The pseudo- 
diphtheria bacillus, when present, cannot be distinguished micro- 
scopically from the true organism, yet this difficulty is liable to 
arise when cultures are made. In such a condition, where pseudo- 
diphtheria bacilli are present only, the inoculation of animals 
appears to give the only positive evidence of diphtheria. 

Pharyngomycosis Leptothricia. — The term pharyngomy- 
cosis leptothricia has been apphed to the peculiar formation of 
horny-like, white tufts in and about the tonsils, on the walls of 
the pharynx, and on the base of the tongue. Recently these white 
patches and tufts have received special attention, and it has been 
proved that many of them are examples of keratosis; others, how- 
ever, deserve the term mycosis pharyngea leptothricia. The first 
clear description of the latter condition appeared from the pen 
of B. Frankel.* Siebenmann contributed an exhaustive and 
admirable paper on this subject in 1895. 

Collection.^Remove a small portion of one of these patches 
by means of a small forceps, smear thinly upon a slide, fix by 
heat, and stain with a solution of iodopotassic iodid. In a number 
of instances the Leptothrix buccalis will be found to be stained a 
bluish-red color (Fig. 193). This organism may also be recov- 
ered from the tartar of the teeth and from the mucous mem- 
brane surrounding the white patches. 

Keratosis. — Recently C. W. Richardson f has described in de- 

* "Berlin Med. Soc," 1873. f "Amer. Jour. Med. Sci.," Oct., 1902. 



TONSILLAR MEMBRANE. 



461 



tail these patches of so-called mycotic disease of the pharynx. In 
his paper Richardson states that in a large percentage of cases 
the condition is a true keratosis, and that the occurrence of the 
leptothrix in the patches is either accidental or physiologic, but that 
the organism bears no causal relation to the condition. Although 
there are probably various types of the Leptothrix buccalis, and 
while the earlier writers regarded this organism as the sole cause 
of the condition, more recent investigators (A. Brown Kelly) 
regard the disease as possibly due to bacteria other than the 
leptothrix. According to this view the bacteria induce certain 
changes in the lacunar epithelium (epithelial buds), which e Ventu- 




ris- 193- — Leptothrix buccalis from the sputum of a phthisical patient. Fresh specimen treated 
with lactic acid and Lugol's solution (X about 300). 



ally result in the production of the white masses and horny quills. 
The leptothrix filaments are found in large numbers in specimens 
obtained from the tonsils, tongue, and nasopharynx. Organisms 
have been isolated from all these situations which have been prac- 
tically identical with those recovered from the white patches pre- 
viously described. 

Cultures from the Throat. — Loffler's blood-serum will be 
found most serviceable for the cultivation of all bacteria common 
to the buccal secretion (see outfit. Fig. 194). Place the patient 
in a bright light, direct him to open his mouth well, or if a child 
see figures 195 and 196, and by means of a spoon or a tongue 




Fig. 194.— Health Department outfit for diphtheria diagnosis. A pasteboard box containing 
a swab-tube and a serum-tube, both with etched surface on which to write the name anc 
address of patient, etc. (Gorham). 




Fig. 195. — Method of holding a child Fig. 196. — Making culture from throat. Left 
when examining the throat : a blanket hand of nurse on child's occiput, 

is wrapped to hold the arms by the side. 

462 



TONSILLAR MEMBRANE. 



463 



depressor obtain a clear view of the throat. Place a small amount 
of sterilized cotton upon a platinum needle (Fig. 197); draw the 
cotton over the false membrane of the tonsil^ 
pharynx, or buccal mucosa, applying sufficient 
pressure to dislodge as much of the membrane 
as possible. Carry this cotton and its contained 
secretion into the culture-tube containing Loffler's 
blood-serum (Fig. 198), and smear the cotton 
over the entire surface of the medium. Cork 
tightly with the cotton stopper and place the 
tube in an incubator for twenty-four hours, when 
examine for colonies of the Klebs-LofBer bacillus 
and for other bacteria. In case of diphtheria the 
Klebs-Loffler bacillus may be present in a pure 
culture, but it is the rule to find it in conjunc- 
tion with other organisms. At times the strepto- 
coccus may be the predominant organism, and a 
common finding is but few Klebs-Loflfler bacilli 
with many colonies of staphylococci and of a large 
diplococcus. The streptothrix is also commonly 
encountered, and may appear in pure cultures in 
cases of pharyngomycosis. 

Staining. — Remove one of the colonies that 



fi 




Fig. 197. — Rosen- 
berger's holder for 
platinum needle. 



Fig. 198. — Method of holding tubes during inoculatic 



may have developed at the end of twenty-four hours by means 
of a platinum needle, and spread it thinly upon a slide, fix by 
heat, and stain for from three to five minutes with Loffler's 



464 BUCCAL SECRETION. 

methylene-blue solution. Diphtheria bacilli are seen to stain 
in a rather characteristic manner, their extremities staining deeply 
(Plate 31). 

Other pathogenic bacteria are also stained by this solution. 
Tuberculous conditions of the throat are to be recognized by 
staining the secretion for the tubercle bacillus (page 438), since 
culture studies of this organism from the buccal secretion are 
impracticable. 



CHAPTER VII. 
THE NASAL SECRETION. 

Naked-eye Appearance. — In health the nasal secretion is 
comparatively scanty, but in certain diseased conditions, either 
acute or chronic, it may be profuse. Normally the secretion is a 
clear, tenacious, odorless liquid, having a saline taste, and pre- 
senting a slight beaded froth. It is composed principally of 
mucus. Microscopically this secretion is found to contain epithe- 
lial cells in abundance, leukocytes, and fungi. Some epithelial 
ceUs show cilia, while others exhibit the various degenerative 
processes. 

Reaction. — The reaction of the nasal secretion is alkaline. 

Rhodan. — Rhodan may be present in the nasal and in the 
buccal secretions. It is detected by placing a drop of the secretion 
on filter-paper that has been previously colored yellow by a solution 
of ferric chlorid in hydrochloric acid. If rhodan is present, the 
yeUow paper will turn red. Keller * discovered that rhodan is 
present in the nasal secretions of children two and three months 
old, but not in their saliva. 

Pathologic Secretion. — In acute inflammatory processes of 
the nasal mucosa the secretion at first is diminished in amount, 
but following this stage it becomes profuse. In the latter condi- 
tion numerous epithehal cells, together with a number of bacteria, 
may be found. Pus is present only when ulceration ensues, and 
its quantity bears a direct relation to the degree of ulceration. 
Chronic suppurative processes may affect both the nasal mucosa 
and the accessory air-spaces, such as the antrum, the ethmoidal 
air-ceUs, etc. 

Hay-fever. — During the course of hay-fever the nasal secre- 
tion will be found to vary greatly at different hours of the day, 
depending upon the occurrence of the characteristic paroxysms 
of the disease. Early in one of these paroxysms the nasal secretion 
is lessened, but after the attack of sneezing the secretion becomes 
profuse. Microscopically the nasal secretion in this disease re- 
sembles that of an acute inflammation and often contains red 
blood-cells. 

* " Miinchener med. Wochenschr.," Nov. 13, 1000. 
30 465 



466 THE NASAL SECRETION. 

Tuberculosis. — Tubercle bacilli may be found in the nasal 
secretion whenever there is a tuberculous ulceration of the naso- 
pharynx. In my experience it has been rather common to find 
this organism present in the discharge from the nose in cases of 
large pulmonary cavities and in cases of tuberculous laryngitis. 
The finding of this bacillus in the nasal secretion is, therefore, of 
limited clinical value. 

Meningitis. — The cerebrospinal fluid may escape into the 
nasal cavity as a result of fracture of the base of the skull. Cere- 
brospinal fluid has also been detected in the nasal secretion in 
cases of cerebral tumor and of caries of the bones of the skull. 

Detection. — The presence of this fluid may be detected in the 
nasal secretion by the fact that it is practically free from albumin 
and that it contains a questionable body which is capable of 
reducing Fehling's solution. 

The Diplococcus intracellularis of Weichselbaum (Fig. 213) 
may be found in the nasal secretion early in the course of epidemic 
cerebrospinal meningitis. This organism is said to have been found 
in the nasal secretion in healthy persons, but my experience does 
not confirm this statement. Out of twelve fatal cases of epidemic 
cerebrospinal meningitis I was able to detect the Diplococcus in- 
tracellularis in the nasal secretion in eight, both in cover-glass 
preparations and by culture. In staining for this organism a 
portion of the mucus or mucopus is smeared in a thin layer upon a 
shde, fixed by heat, stained for fifteen seconds with a solution 
of anilin-gentian-violet, and washed in water. Apply Gram's 
solution for one minute and alcohol until all the violet color dis- 
appears; wash again in water, and stain for two minutes with a 
saturated alcoholic solution of Bismarck-brown. The Dip- 
lococcus intracellularis will be found to be stained brown; the 
nuclei of the pus-cells and leukocytes, a mahogany-red; while the 
protoplasm of the cells will be stained a Hght brown. The menin- 
gococcus is often found within the bodies of the pus-cells, — 
a feature also characteristic of the gonococcus, — but, on the 
other hand, many extracellular diplococci are also present 
(see Meningitis). Without such an examination it is unwise 
to venture a positive diagnosis. 

Glanders. — During the course of glanders the nasal secretion 
is most likely to contain the Bacillus mallei in great numbers. 

Ozena. — In ozena the nasal secretion is said to contain many 
large diplococci, and, according to Lowenberg, this finding is 
fairly constant. Schlafrig* recovered a pure culture of the 

* "Wien. klin. Wochenschr.," Oct. 17, 1901. 



FUNGI. 467 

Micrococcus tetragenus in this disease. Fungi (Oidium albi- 
cans), cocci, and bacilli may also be found. 

Klemperer and Sheier, in a rather exhaustive monograph upon 
the bacteriology of ozena and rhinoscleroma, conclude that the 
so-called bacillus of ozena resembles closely the bacillus of Fried- 
lander (Fig. 188), and these authors beheve that the latter organism 
becomes plentiful in the nasal secretions during the course of ozena.* 
In a few instances the tubercle bacillus has been recovered from 
the discharge in cases of ozena. 

Leprosy. — Whenever leprosy involves the nasal cavity or the 
adjacent tissues, lepra bacilli may be found in the nasal secretion. 
They may be detected by the method described on page 112. 

Plague. — In the pneumonic form of bubonic plague the nasal 
secretion may be found to contain the plague bacillus, but this 
finding is of but little importance, since the organism is readily 
recovered from other situations (see Plague, page 114). In plague 
pneumonia the sputum contains plague bacilli (Plate 31). 

Pneumonia. — It is not uncommon to find the pneumococcus 
in the nasal secretion during the course of acute lobar pneumonia, 
and I have repeatedly isolated it from the nasal cavities of healthy 
persons. In one instance I recovered the bacillus of Friedlander 
from the nasal secretion in a case of lobar pneumonia. 

Influenza. — The influenza bacillus may be detected in the 
nasal secretion early in the course of influenza. The bacilK 
appear as very slender rods which stain readily with carbolfuchsin 
(see Sputum). 

Typhoid Fever. — During the course of typhoid fever many 
microorganisms may be obtained from the nasal secretion, and 
while the typhoid bacillus is at times present, the finding is of no 
clinical importance. Streptococci, diplococci, and bacilli are also 
present. The nasal secretion is likely to contain many red blood- 
cells, but the other evidences of inflammation are wanting. 

Crystals. — Charcot-Leyden crystals (Fig. 189) are often to be 
seen in the nasal secretion, as are also crystals resembling the 
triple phosphates in appearance. 

Fungi. — Molds are occasionally recovered from the nasal 
secretion, and a few records have appeared in the hterature in 
which the thrush fungus and the aspergillus have been detected. 

Entozoa. — Ascarides and oxyurides are reported as having 
been found in the nasal secretion. The larvae of certain insects 
have also been found in the nasal cavity, but have rarely been 
detected in the discharge. 

* "Zeit. f. klin. Med.," vol. -Iv, pts. i, 2. 



CHAPTER VIII. 
DISCHARGES FROM THE EAR AND EYE. 

THE EAR. 

During the past few years the discharge from the middle ear 
has been studied in connection with both acute and chronic in- 
flammations of the middle ear, as well as with catarrhal processes 
of the external auditory canal. Among the organisms commonly 
encountered in this situation should be mentioned the pneumococ- 
cus, the Streptococcus pyogenes, both of which are commonly 
associated with acute otitis media, the Staphylococcus pyogenes 
albus, the Staphylococcus pyogenes aureus, the Bacillus pyocy- 
aneus, the bacillus of Friedlander, and the Bacillus coli communis. 
During the course of epidemic cerebrospinal meningitis the Dip- 
lococcus intracellularis may be found in the auditory discharge, as 
was observed in a case studied at the Philadelphia Hospital. The 
typhoid bacillus has been recovered from the auditory discharge 
in cases in which otitis media was found to comphcate typhoid 
fever. When diphtheria involves the middle ear, the diphtheria 
bacillus may be detected in the auditory exudate. The tubercle 
bacillus has also been found in cases in which there is tuberculous 
involvement of the ear or the adjacent structures. During the 
course of influenza the bacillus of influenza may be found within 
the middle ear or in the pus discharge from the canal. There 
appears to be some question as to the exciting cause of acute otitis 
media, and it may safely be said that the laboratory worker is 
seldom called too early to recover the pneumococcus and the 
streptococcus, but, according to the researches of Lermoyez and 
Helme,* otitis media is of monobacillary origin, and the pneumo- 
coccus or the streptococcus is seldom to be found with other 
micro-organisms. At any rate, the disease has not progressed 
far when the pus becomes contaminated with staphylococci, so 
that it is not uncommon to find the latter organism only imme- 
diately after paracentesis. The fact that disease of the ear is 
commonly secondary to disease of the nasopharynx renders it 
reasonable to suppose, at least, that the same organisms are con- 
's^ "Annal. d. Mai. de I'Oreille," 1895. 
468 



PARASITIC INFLAMMATION OF THE EAR. 469 

cerned in the production of the two conditions, and that they 
may be recovered from the pharyngeal and nasal mucosae as well 
as from the middle ear — e. g., during the course of scarlet fever 
streptococci and diplococci may be found in the throat, as well 
as in the discharge from the ear. 



PARASITIC INFLAMMATION OF THE EXTERNAL AUDITORY 

CANAL. 

(Otomycosis; Myringomycosis aspergillina.) 

Mycosis of the external auditory canal is commonly of parasitic 
origin, and, in a great many instances, this condition is excited 
by the development of a rather common fungus, the Aspergillus 
niger, although other species of this organism have also been 
found — Aspergillus fiavus and fumigatus. In addition to these or- 
ganisms the Vesticillium graphii, Aspergillus fumigatus with grass- 
green conidia, Aspergillus nidulans, Ascophora elegans, Mucor 
corymbifer, Eurotium malignum, Mucor septatus, and the Peni- 
cillium minimum have been recovered from the external auditory 
canal. 

Detection. — Remove a small portion of the mycotic debris 
and spread it thinly on a slide; add a small drop of water and 
apply a cover-glass. When studied under a one-fourth or one- 
sixth objective, many small, tape-hke structures (hyphse) may be 
seen (Plate 21), many of which support a spheric, granular body at 
one extremity (sporangium). Surrounding the sporangium several 
small spheric bodies (spores) are usually seen, which have been 
detached during manipulation (Plate 21). The various forms 
of aspergillus may be known partly from the color of the growth 
they produce, which depends somewhat upon their conidia. 
The Aspergillus niger produces a blackish or dark-brown growth; 
A. flavus, a yellowish or green growth, which is also produced by 
the A. glaucus; while a dull-gray or grayish-brown growth is 
characteristic of the A. fumigatus. I have found that the culture- 
medium and the degree and character of the Hght influence the 
color of the growth of the aspergillus materially — e. g., when 
grown under a red, green, or blue glass the characteristic color of 
the fungus was greatly changed. 

Sterigmatocystis Candida. — S. E. Cook* reports a case in 
which this fungus was found in the external auditory canal. The 
author claims his case to be the first in which this parasite (Fig. iqq) 
was proved to be the cause of auditory mycosis. 

* "Amer. Med.," Dec. 5, 1Q03. 



470 



DISCHARGES FROM THE EAR AND EYE. 



LARV^ IN THE AUDITORY CANAL. 

Living larvae of dipterous insects may be detected in the human 
external auditory canal. W. E. Baxter,* in addition to reporting 
a case, makes reference to a number of instances where such 
larvae have been recovered from this situation. As early as 1871 
C. J. Blake contributed an interesting monograph upon this sub- 
ject,! 2,nd several additional reports 
of the recovery of living larvae from 
the external auditory canal have 
also crept into the literature, 
among which it may be well to 
make special mention of a report 
by C. W. Richardson.J In Rich- 
ardson's case there was a blood- 
stained purulent discharge from 
both ears. One hving larva of a 
fly was removed from the right 
external auditory canal; and from 
the left canal two living worms 
were removed. The age of the 
child from whom these larvae were 
"B removed was four months. 

THE EYE. 

In health the secretion of the 
conjunctiva concerns us but Httle, 
although when studied microscop- 
ically it will be found to contain 
a few epithelial cells and small 
corpuscles. During the course of 
inflammatory processes of the con- 
junctiva, on the other hand, the secretion may be greatly in- 
creased and may at times become purulent. 

Again, it may remain comparatively clear, although it contains 
a profusion of bacteria. 

Gonorrheal Conjunctivitis. — Early during the course of 
gonorrheal conjunctivitis a variable quantity of pus may be seen 
exuding from between the folds of the swollen conjunctiva. 




Fig. 199. — Sterigmatocystis Candida 
A, Fertile hypha ; B, terminal vesicle 
C, sterigmata, one showing chains of co 
nidia. 



* "Arch, of Otol.," vol. xx, No. i. 

t "Arch. Path, and Otol.," vol. ii, pp. 37-44, No. 2 

j "Arch, of Otol.," 1895, vol. xxiv, Nos. 3, 4. 



THE EYE. 471 

Collect a small drop of this discharge upon a platinum needle 
or upon a tooth-pick and smear it thinly over a sHde; fix the speci- 
men by passing it through the flame of a Bunsen burner, and then 
stain for the gonococcus (see Gonorrhea, page 494). Early during 
the course of the disease, when the pus is profuse, it has been 
my experience to find a pure culture of the gonococcus; but after 
the application of judicious treatment, especially silver-nitrate solu- 
tion, the gonococci lessen in number and at times other bacteria 
(streptococci and staphylococci) appear in the discharge. In fact 
it is not uncommon, late in the disease, to find a rather large 
quantity of purulent discharge which, upon microscopic examina- 
tion, is found free from bacteria. 

Gonorrheal conjunctivitis should probably be considered as a 
variety of ophthalmia neonatorum, although not all cases of this 
condition are found to be due to infection with the gonococcus. 
Indeed, I have examined the pus from the conjunctiva of a number 
of children in which it was impossible to detect gonococci. 

When judicious treatment has been instituted early, it may 
be difficult to detect gonococci in the discharge after the fourth or 
the fifth day of the disease ; yet the exact stage at which gonococci 
disappear from the pus is apparently influenced by the individual 
resistance of the patient, the type of infection, and the treat- 
ment. 

The characteristic feature of the gonococcus is that it is situated 
within the pus-cells and the epithelium. Early in the course of 
ophthalmia many extracellular cocci are seen, and, in fact, these 
may appear in rather dense aggregations, resembling the staphy- 
lococcus (Plate 34). The appearance of the streptococcus or of 
the staphylococcus in the pus may be regarded as a precursor 
of the disappearance of the gonococcus. 

Keratitis. — In cases of keratitis various micro-organisms may 
be detected in the discharge from the conjunctivae, and at times 
the same organisms are recovered from the nasal passages. The 
following organisms have been found in this connection : Staphy- 
lococci, streptococci, Pfeiffer's capsulated bacillus, pneumococci, 
Bacillus pyogenes foetidus. Bacillus coli communis, the Bacillus 
pyocyaneus, diplobacillus, ozena bacillus, influenza bacillus, and 
tubercle bacillus. Certain fungi are also to be found, among which 
the Aspergillus fumigatus represents the one of pathologic im- 
portance. Uhthoff recovered lepra bacilli from the conjunctiva 
in a case of leprosy, and Posey found the same organism in a case 
of leprosy with chronic conjunctivitis.* The micro-organisms 
present in a given case depend upon the character of the ulcer in 

* "Jour. Amer. Med. Ass.," Oct. 3, 1903. 



472 DISCHARGES FROM THE EAR AND EYE. 

that case ; a sloughing ulcer may result from one or many bacteria. 
In a number of cases, many of which were studied at the Phila- 
delphia Hospital through the courtesy of Dr. de Schweinitz, I 
found that mixed infection was common. Certain of the ulcers 
produced a discharge which contained the pneumococcus only 
(Fig. 200); other discharges contained pneumococci and staphyl- 
ococci ; while a third series displayed streptococci in addition. At 
the suggestion of Dr. de Schweinitz cultures and smears were 
made from the margins and also from the centers of these ulcers. 
At times the marginal culture was found to contain only 
diplococci, staphylococci, or streptococci, while near the center 
of the ulcer more than one, and at times all, of these organisms 
existed. Occasionally the reverse condition was found to exist. 




Fig. 200. — Diplococcus pneumoniae from ulcer of cornea (obj. B. and L. one-twelfth oil-im- 
mersion) (study through courtesy of Dr. C. A. Oliver). 



In none of the cases studied was I able to detect the pseudo- 
diphtheria bacillus. 

Epithelial cells and a variable amount of tissue debris are to be 
found in the scrapings from corneal ulcers. 

Parasitic Keratitis. — In a case in which keratitis was compli- 
cated by hypopyon a keratotomy released a foreign body which 
was determined to be Hypoderma bovis, larva of the warble fly.* 

Trematodes of the Eye. — Thus far there appear to be 
authentic records of but two instances where trematodes have 
invaded the human eye. These parasites have been referred to 
under a variety of names, and from the number of references to 
this subject one might at first glance suppose that trematodes were 
commonly found in this situation. Stiles has discussed at length 
the limited importance of this parasite in its relation to man, and 
has considered the trematodes invading the eye (Plate 32) under 

* "Hygeia," Sept., 1901. 



PLATE 32. 





, t,-.^^- 



''^^^^Hv 






•^ 



>^^.:y^^^^iP 




Agamodistomum Ophthalmobium. 

I-, Ventral view; 2, dorsal view; 3 and 4, two other views in different stages 
of contraction (after von Amnion). 



THE EYE. 473 

the terms Monostomulum lentis and Agamodistomum ophthal- 
mobium.* 

Keratomycosis. — i\ccording to Ball,t less than a dozen 
cases of this affection are described in the literature. The mycotic 
area appears as small black bodies within the substances of the 
cornea. Upon removal from the cornea the mass may be crushed 
upon a slide, a drop of water added to it, and the specimen brought 
into focus under a one-fourth or a one-sixth objective. It will be 
found to consist for the most part of mycelial threads, a few of 
which show sporulation (sporangia), spores, and a variable number 
of pus-corpuscles (Fig. 201). This fungus, when present in the 
black bodies, is suggestive of Aspergillus niger, although I am 
not aware that this organism is commonly the cause of pathologic 



I 




2 


at 








4 


^ -- 3 



Fig. 201. — Microscopic appearance of a section of the growth in aspergillar keratitis : i, 
Epithelial surface of cornea ; 2, sporangium ; 3, mycelium ; 4, leukocytes or pus-cells 
(Ball). 

conditions. On the other hand, the Aspergillus fumigatus, which 
usually produces a brownish or yellowish-green growth, is highly 
pathologic for animals. Osterroht } reports a similar case. 

In so far as I have been able to learn from, the literature, the 
organism found in aspergillous keratitis is probably one of these 
fungi, though there is no record of cultural studies of this parasite 
(see Culture of the Aspergillus, page 469). In Ball's cases the 
black masses removed from the cornea were sectioned. 

Keratoconjunctivitis. — In keratoconjunctivitis it is fair to 
presume, at least, that the same etiologic factors that have been 

* U. S. Department of Agriculture, Bureau of Animal Industry. Bulletin 
No. 35. 

f'Amer. Med.," July 6, i9oi,p.3i. J "Berliner klin.\\ ochen.," Feb. 13. 1005. 



474 



DISCHARGES FROM THE EYE AND EAR. 




Fig. 202. — staphylococcus pyogenes aureus in 
exudate from corneal abscess. Observed at Phila- 
delphia Hospital (obj. Queen one-twelfth oil-immer- 
sion). 



described under the head of keratitis are active. When the dis- 
ease is of a carcinomatous 
nature, a portion of the 
growth may be removed 
for pathologic study; but 
scrapings from the con- 
junctiva have never given 
sufficient evidence to en- 
able me to make a posi- 
tive diagnosis. 

Abscess of the Cor- 
nea. — In four cases of 
abscess of the cornea 
Staphylococcus aureus was 
present in two (Fig. 202); 
the Staphylococcus pyog- 
enes, Staphylococcus 
pyogenes albus, and the 
Streptococcus pyogenes 
were found in the third, 
and the pneumococcus 
and a staphylococcus of a questionable nature were present in 
the fourth. In these cases the pus was released by the surgeon 

and collected as it exuded 

from the cornea. In this 
connection tuberculosis of 
the cornea and suppura- 
tive keratitis should be 
mentioned, as they are 
also of bacterial origin. 

Diphtheric Conjunc- 
tivitis. — The exudate 
from a case of diphtheric 
conjunctivitis may show 
broken-down epithelial 
cells, leukocytes, debris, 
and a growth of strepto- 
cocci (Fig. 203). A false 
membrane may result, ac- 
cording to some authors, 
from the development of 
the leptothrix (Fig. 193). 
This organism may ac- 
cumulate to form a rather dense mass in the conjunctival tissue 




Fig. 203.— Streptococcus pyogenes from the exu- 
date during acute membranous conjunctivitis. Ob- 
served at Philadelphia Hospital (obj. Queen one- 
twelfth oil-immersion). 



THE EYE. 



475 



This mass, subsequently becoming calcified, forms the so-called 
"tear stone." In in- 
stances in which the 
Klebs-Loffler bacillus is 
found in the scrapings 
and in the cultures from 
the conjunctiva the con- 
dition should be regarded 
of diphtheric nature. 

Caution. — A fact ever 
to be borne in mind is that 
the diphtheria bacillus is 
not essential to the pro- 
duction of a false mem- 
brane. 

Trachoma. — In tra- 
choma the granular lids 




Fig. 204.— Morax-Axenfeld diplobacillus from 
conjunctival exudate during course of subacute con- 
junctivitis. Patient observed at Philadelphia Hos- 
pital (obj. B. and L. one-twelfth oil-immersion). 



have not been proved to 
be due to the diplococcus 
of Sattler or of Michel; 
' ' neither has the trachoma- 
coccus been identified; indeed, some observers (Mutermilch) 
deny its existence" (de Schweinitz). Noiszewsky has described 

a fungus which, in many 
respects, resembles the 
Microsporon furfur, and 
has found this organism 
pathologic for rabbits. 
Pfeiffer has described a 
protozoon in connection 
with trachoma, but the 
true organism upon which 
this disease depends is not 
definitely known. 

Acute Infectious Con- 
junctivitis. — Koch has 
described a specific ba- 
cillus which he found com- 
monly associated with the 
conjunctival secretion in 
acute infectious conjunc- 
tivitis. Morax has also 
studied this organism in Europe, as well as a diplococcus (Fig. 
204). It has been extensively studied in America by Dr. Weeks, 




Fig. 205. — Koch-Weeks' bacillus from conjunc- 
tival exudate at third day of epidemic conjunctivitis 
(obj. Spencer one-twelfth oil-immersion). 



476 DISCHARGES FROM THE EAR AND EYE. 

of Xevs- York. According to Koch's description, this bacillus 
resembles the organism of mouse septicemia in certain respects. 
It measures from one to two u. in length by 0.25 a in breadth, 
and stains readily with the ordinary anihn dyes. The Koch- 
AVeeks' bacillus (Fig. 205) grows well upon the addition of 
hemoglobin to the surface of the culture-medium. The bacillus 
of influenza (Fig. 187) has been suggested as being identical 
with this organism. At times this may be the only organism 
present in the conjuncti^-al secretion, although it is commonly 
associated with a bacillus resembhng that of diphtheria (xerosis 
bacillus). It has been claimed by Rimovitch * that the bacillus 
of acute infectious conjunctivitis is identical with the influenza 
bacillus. 

Parasitic Cysts. — The small hard sacs of the eyelids have 
been studied by Hunsche,t who found that omitting young chil- 
dren, in whom this disease is not usual, 92.5 per cent, of cases are 
due to the Demodex fofliculorum, a minute parasite known to 
infest the sebaceous folhcles of man and of certain animals. 
This parasite does not, as a rule, excite appreciable inflammation. 

* '"Russki Archiv Pathologii," etc., vol. xii. Xo. 2. 
j '■ ^liinchener med. "Wochenschr.." Nov. 6, 1900. 



CHAPTER IX. 
SECRETION OF THE GENITAL ORGANS. 

SEMEN. 

The ejaculated secretion of the male organs of generation is 
derived from a number of sources : the testicle, the prostate gland, 
the seminal vesicles, Cowper's glands, and the glands of Littre. 
When there is an inflammatory process of any or all of these 
glands or of the genital mucosa, the secretion may present features 
which may vary according to the pathologic condition present. 
Again, a disproportionate activity of one gland or set of glands 
often results in an abnormal appearance of the secretion. 

Method of Collection. — Direct the patient to prepare a 
vaselin bottle which is provided with a well-fitting cork. If the 
semen is to be collected at the time of sexual intercourse, the penis 
should be withdrawn just before ejaculation and the semen 
allowed to escape into the bottle. The bottle should be corked 
tightly and kept warm (37° C. — 98.6° F.) until a careful study 
has been completed. Semen collected after masturbation or after 
an involuntary emission is equally valuable for study. When it is 
necessary to convey the semen for a considerable distance I have 
found the following plan to serve well for keeping the spermatozoa 
active: Place a quantity of fresh semen in a bottle two inches 
long by one-half inch in diameter and cork tightly. Attach a 
string of sufficient length to the neck of this bottle, so that when 
suspended from a button on the trousers, the bottle will hang 
against the skin of the inguinal region. In this way the semen is 
kept warm and may be carried for hours without the spermatozoa 
losing their motility. 

Characteristics. — The seminal fluid when first ejaculated is 
a thick, white, bluish-white, or yellowish, opaqlie, tenacious, semi- 
gelatinous fluid of an alkaline reaction. Upon standing exposed 
to the air it soon becomes opaque and gives off a characteristic 
sweetish odor. Fresh semen will be found to sink when placed in 
water, collecting as a gelatinous mass at the bottom of the vessel. 
When shaken with water, the cellular elements arc found to be 
distorted. 

477 



Horse. 


Bull. 


81.9 


82.1 




15-3 


16.45 






2.2 


1.61 


2.6 



478 SECRETION OF THE GENITAL ORGANS. 

Chemistry, — According to the analysis of Vauquelin and 
Kollicker, mammalian semen is composed of the following : 

Man. 

Water 90.0 

Albuminous material 

Extractives 6.0 

Ethereal extract 

Mineral substances 4.0 

The mineral constituent ordinarily found in semen is calcium 
phosphate. 

Microscopic Study. — Place a drop of the semen upon a slide 
and permit it to remain exposed to the air for a short time; then 
apply a cover-glass and examine microscopically for the so-called 
Charcot-Leyden crystals (Fig. 189). Other needle-like crystals, 
which are probably phosphates, may also be found. Warm a 
slide to body-temperature and place a drop of sem-en upon its 
center. Repeat the warming process from time to time, carrying 
the slide to the microscope between each heating and bringing it 
into focus under a one-sixth or a one-eighth objective. When thus 
examined, the semen will be seen to contain many actively motile 
bodies which, upon careful focusing, are best described by the 
accompanying illustrations (Plate 33). 

Spermatozoon. — The male cell, or spermatozoon, is of 
minute size, and in its locomotive energy and vitality resembles a 
flagellate monad. Anatomically the spermatozoon is a true cell; 
it is composed of a head, a middle piece, and a tail or flagellum. 
The head of the spermatozoon corresponds to the nucleus of a 
somatic cell, and is, therefore, composed principally of chromatin. 
The middle piece contains the centrosome. The tail, which is 
actively motile in the living cell, contains a central axial filament. 
This axial filament starts from the centrosome in the middle piece 
and runs through the entire length of the tail. Human spermato- 
zoa will be found to resemble the spermatozoa of certain other 
mammals* in many respects (see Plate 33, in which a comparative 
study of the spermatozoa of man, domestic animals, and rodents 
is illustrated). 

In studying the spermatozoa of the mastiff I noticed the striking 
resemblance they bore to those of man. I also found that if the 
spermatic fluid were allowed to stand for a time, even staining did 
not furnish sufficient evidence to enable me to distinguish beyond 
question the spermatozoa of man from those of the dog. Only 
when careful measurements were employed was the differential 
diagnosis possible. A fact ever to be borne in mind is that these 

* Boston, "Jour. App. Mic," vol. iv, No. 7, p. 1360, Rochester, N. Y. 



PLATE 33. 




-Q s 



to 
o 
-a 



PLATE 33— (Continued' 




g 2 



< 43 



CO ^ 

03 



SEMEN. 479 

measurements may vary slightly in different persons and in ani- 
mals, and even in spermatozoa from the same specimen of semen. 
In this connection I am prompted to offer the following table of 
measurements, obtained by personal observations : 

SPERMATOZOA OF MAMMALS. 

]Man. 

Total length 0.051-0.058 mm. (0.002 -0.0022 in.) 

Length, head 0.004-0.006 mm. (0.0001-0.0002 in.) 

Width, head 0.003-0.004 mm. (o.oooi-o.oooi in.) 

Length, tail 0.041-0.053 mm. (0.0016-0.002 in.) 

Dog. 

Total length 0.067-0.074 mm. (0.0026-0.0028 in.) 

Length, head 0.004-0.008 mm. (0.0002-0.0003 ^^■) 

Width, head 0.003-0.002 mm. (0.0001-0.0001 in.) 

Length, tail 0.059-0.067 mm. (0.0023-0.0026 in.) 

Rabbit. 

Total length 0.051-0.066 mm. (0.002 -0.0025 ^^■) 

Length, head 0.006-0.009 mm. (0.0002-0.0003 in.) 

Width, head 0.003-0.004 mm. (0.0001-0.0001 in.) 

Length, tail 0.045-0.058 mm. (0.0017-0.0022 in.) 

Horse. 

Total length 0.064-0.067 mm. (0.0025-0.0026 in.) 

Length, head 0.006-0.008 mm. (0.0002-0.0003 ^^•) 

Width, head 0.003-0.004 mm. (0.0001-0.0001 in.) 

Length, tail 0.054-0.06 mm. (0.0021-0.0022 in.) 

Bull. 

Total length 0.087-0.093 mm. (0.0033-0.0036 in.) 

Length, head 0.009-0.009 mm. (0.0003-0.0003 in.) 

Width, head 0.006-0.006 mm. (0.0002-0.0002 in.) 

Length, tail 0.077-0.083 mm. (0.003 -0.0032 in.) 

Mouse. 

Total length 0.12 -0.158 mm. (0.0046-0.0061 in.) 

Length, head 0.008-0.009 mm. (0.0003-0.0003 in.) 

Width, head 0.003-0.004 mm. (0.0001-0.0001 in.) 

Length, tail o.i 12-0. 138 mm. (0.0043-0.0057 in.) 

Sheep. 

Total length 0.083 rnni. (0.0032 in.) 

. Length, head 0.009 mm. (0.0003 i"-) 

Width, head 0.006 mm. (0.0002 in.) 

Length, tail 0.074 mm. (0.002S in.) 

Cat. 

Total length 0.058-0.074 mm. (0.0022-0.002S in.) 

Length, head 0.004-0.007 mm. (0.00 1 -0.0002 in.) 

Width, head 0.003-0.003 mm. (0.0001-0.0001 in.) 

Length, tail 0.053-0.066 mm. (0.002 -0.0025 ^^■)' 



480 SECRETION OF THE GENITAL ORGANS. 

White Rat. 

Total length 0.225-0.238 mm. (0.0087-0.0092 in.) 

Length, head 0.012-0.016 mm. (0.0004-0.0006 in.) 

Length, tail 0.209-0.222 mm. (0.0081-0.0086 in.) 

Guinea-pig. 

Total length 0.113-0.138 mm. (0.0053-0.0057 in.) 

Length, head 0.006-0.012 mm. (0.0006-0.0004 ^^■) 

Width, head 0.007-0.01 1 mm. (0.0004-0.0004 in.) 

Length, tail 0.125-0. 132 mm. (0.0048-0.0051 in.). 

Semen also contains epithelial cells, hyaline bodies, and a 
few granular bodies which are not unlike starch-granules in 
appearance. Leukocytes are always present, and a few red 
blood-cells are usually demonstrable. 

Stain. — Spermatozoa stain readily with the ordinary anilin 
dyes. 

PATHOLOGY OF THE SEMEN. 

In this country a careful study of the semen is sadly neglected, 
and in a case of a sterile marriage the fault is usually ascribed 
to the female. According to Kehrer, however, spermatozoa are 
absent from the semen in 40 per cent, of the cases of sterile mar- 
riages (azoospermism). 

My own experience in a rather large number of cases does not 
accord with Kehrer's findings, although I have found a number of 
instances in which sterility was dependent upon some pathologic 
state of the semen. In many instances no spermatozoa were 
present (azoospermism) ; in others many well-formed spermatozoa 
were found, but they were devoid of motility; and in a third 
group of cases the heads and tails of the spermatozoa were 
separated. While these three findings have been common in 
my experience, I have never been able to learn from the genito- 
urinary specialist upon what pathologic conditions these changes 
depend. Spermatozoa are absent from the semen during con- 
valescence from acute febrile conditions (typhoid fever), and in 
such chronic conditions as valvular heart disease, severe anemia, 
tuberculosis, and other states in which the general vitahty of the 
individual is greatly reduced. In a number of cadavers examined 
postmortem I was unable to recover spermatozoa from the vas 
deferens. 

Bacteria. — The semen may contain the gonococcus, the 
Staphylococcus pyogenes, the streptococcus, and, rarely, the 
tubercle bacillus. 



VAGINAL SECRETION. 48 1 



VAGINAL SECRETION. 

In health the vaginal secretion is scanty in amount — merely 
sufficient to keep the mucous membrane lubricated. It is clear 
or at times opalescent, semiliquid, and is composed for the greater 
part of mucus and epithelial debris. It is acid in reaction. 



MICROSCOPIC STUDY. 

Microscopically a large amount of cellular debris will be 
found, entangled in the meshes of which are epithelial cells, 
mononuclear leukocytes (large), mucus-corpuscles, and bacteria. 

The bacteria to be found in the vaginal secretion concern us 
but little, since a profusion of micro-organisms may be present 
without causing the patient any inconvenience. Doderlein 
regards his special bacillus as the only organism constantly 
present in the normal vaginal secretion. This organism pos- 
sesses the faculty of inducing a marked acid fermentation of 
sugar. Doderlein's claims have not been substantiated by the 
works of other equally careful investigators (Kronig and Menge). 
These observers have found cocci and bacilli present in vaginal 
secretions which were apparently normal. Such organisms 
belong to a class of anaerobes known to be non-pathogenic. 
It will be found that a variety of organisms may be cultivated 
from the lower portion of the vagina, while an entirely different 
group of organisms are obtained from the upper portion of the 
canal and from the cervix of the uterus. 

Collection. — Separate the labia well and lift a small amount 
of the secretion by means of a platinum needle. Transfer this 
to the center of a clean slide, and smear thinly over the surface 
of this slide by means of a second slide (see Blood-smears, page 
35). A number of sHdes may be prepared in this way by the 
gynecologist or by the general practitioner. Place the specimen 
surface of slide No. i up, and upon it place two bits of match- 
sticks. Rest the second slide, specimen surface down, upon these 
sticks. In this way a number of slides may be piled together so 
as to prevent the specimens from touching. The slides should 
be _ wrapped in paper and sent to the laboratory for exami- 
nation. When it is desired to transfer the vaginal secretion to the 
laboratory in liquid form. Dr. W. Easterly Ashton has employed 
the tubes used for the collection of blood (Fig. 44). A small 
syringe is attached to one end of the capillary glass tube by means 
of rubber tubing. The free end of the capillary glass tube is 
brought in contact with the vaginal secretion, which is then drawn 
31 



482 SECRETION OF THE GENITAL ORGANS. 

into the tube by the suction of the syringe. Remove the rubber 
tubing from the capillary glass tube, and pass the ends of the 
latter through the flame of a Bunsen burner, applying sufficient 
heat to seal it. Place in a test-tube or any suitable receptacle 
and convey to the laboratory. 

Fixing. — Fix all smears of vaginal secretions by heat, either 
by passing them directly through the flame or by heating at a 
lov^ temperature (60° C. — 140° F.) for twenty minutes or more. 

NORMAL AND PATHOLOGIC SECRETION. 

The normal vaginal secretion v^ill be found to contain many 
cocci and bacilli, none of v^hich, however, are pathogenic. In 
many normal secretions a few cocci may be found which in their 




Fig. 206. — Vaginal secretion showing diplococci and smegma bacilli (obj. Spencer one- 
twelfth oil-immersion). 

morphologic and staining properties are practically identical with 
the gonococcus, yet these organisms have not the power to excite 
urethritis in the male. I have found this organism in normal 
vaginal secretions, but have never found it within the protoplasm 
of the pus-cells or epithelial cells in the manner characteristic 
of the gonococcus (Fig. 206). It is almost impossible to 
mistake this organism for the gonococcus, because the latter, in 
a case of acute gonorrhea before treatment has been instituted, 
always occurs in great numbers and pus-cells are often seen 
which contain from 12 to 50 cocci (Plate 34). In a normal 
secretion containing innocent cocci I have never found the pus- 
cells and the leukocytes invaded to this degree; so that while 
the cultivation of the gonococcus is often recommended, it is an 



NORMAL AND PATHOLOGIC SECRETION. 483 

unnecessary proceeding, and, in addition, is most impracticable. 
It is impossible to inoculate animals with the gonococcus. 

Gestation. — During the latter months of gestation it is 
common to find a profusion of batteria in the vaginal secretion — 
bacilli, streptococci, staphylococci, and, occasionally, diplobaciUi 
and streptobacilli are to be seen. In a series of experiments con- 
ducted at the Philadelphia Hospital a number of these organisms 
were isolated from the vaginal secretions of pregnant women and 
a series of animal inoculations made. I was unable, however, 
to produce pathologic lesions with these bacteria. Other ob- 
servers have found that bacteria isolated from the vaginal secre- 
tions were pathologic for animals only when the vitality of the 
animal or of the part employed for inoculation was greatly 
reduced. 

Bactericidal Properties. — Kronig was the first to dem- 
onstrate conclusively the bactericidal properties of the vaginal 
secretion by placing a number of micro-organisms within the 
healthy vagina and observing carefully at what length of time 
the vaginal secretion was capable of destroying them. Kronig 
found that it was impossible to recover the Bacillus pyocyaneus 
in from ten to thirty hours after its introduction into the vagina; 
the Streptococcus pyogenes disappeared after six hours; and the 
Staphylococcus pyogenes after from six to thirty-six hours. 

Prompted by Kronig's investigations, I began a series of 
similar investigations at the Philadelphia Hospital,* and through 
them was able to confirm his work. More attention was directed 
to the effect of vaginal douches in the removal of these bacteria 
from the vaginal secretion. It was found that by douching 
the normal secretion — "the woman's safeguard against puer- 
peral sepsis" — was removed and that the micro-organisms devel- 
oped more rapidly. Furthermore, it was demonstrated that it is 
impossible to remove pathogenic bacteria from the vagina by 
means of antiseptics, but that they were always destroyed by the 
normal secretion when no douche was employed. A number of 
cases of gonorrhea in the female also received study, and it was 
found that cervical gonorrhea did not develop in the Philadelphia 
Hospital when the woman did not receive douches. On the 
other hand, cervical gonorrhea and pelvic trouble frequently 
followed the administration of douches. 

Gonorrhea. — Urethral gonorrhea appears to be a fairly 
common condition, but vaginal gonorrhea must certainly be 
rare — thus far I have seen but a single case. Pus which con- 
tained gonococci has been obtained from the cervix uteri, but this 

* "N. Y. Med. Jour.," June 10, 1S99. 



484 SECRETION OF THE GENITAL ORGANS. 

is a much less common finding than we are led to believe. The 
gonococcus when present in the vaginal, urethral, or cervical 
secretion or in pus, is detected in the manner described for the 
study of this organism (page 494). 

Caution. — It has been my custom to teach that it is unsafe 
to make a diagnosis of gonorrhea in a female after puberty, since 
many other bacteria may be found which are not unlike gonococci ; 
and in view of the great importance of such a diagnosis I should 
be inclined to rely upon the cultivation of the gonococcus, although 
in my own hands even this has not been satisfactory. 

Ulceration of the Cervix. — In cases of ulceration of the cervix 
uteri the vaginal secretion usually contains a number of bacteria, 
and scrapings from the ulcer may show one or more pathogenic 
organisms to be present. These organisms in some cases are 
capable of producing a urethritis in a male who is exposed. 

Carcinoma of the Cervix. — In cases in which there is a 
carcinomatous erosion of any portion of the v^aginal canal masses 
of tissue which have sloughed may at times be recovered. When 
studied under the microscope, these masses are found to be quite 
characteristic of epithelial growths. Carcinoma, however, should 
be diagnosed after a section of the growth and not after exami- 
nation of mere scrapings from the ulcerated surface. 

Diphtheria and Noma. — Diphtheria of the vulva is certainly 
an uncommon condition, and yet it may be encountered. We 
should, therefore, be on guard for such a condition should it arise. 
The false membrane resembles that seen upon the other mucous 
surfaces, and when a portion of it is removed, spread thinly 
upon a slide, fixed by heat, and stained for five minutes with 
Loffler's methylene-blue solution, it will be found to contain a 
varying number of diphtheria bacilh. 

Noma may at times involve the vulva. This condition is 
doubtless parasitic, and since the finding of the diphtheria bacillus 
by Sailer * in noma of the buccal cavity, the scrapings from such 
ulcers should be stained for this organism. 

Animal Parasites. — The Trichomonas vaginalis is com- 
monly seen in the vaginal secretion. It is apparently identical 
with the trichomonas recovered from the feces. This organism 
is not known to excite pathologic changes. It in no way resem- 
bles the spermatozoon (see page 478). 

Oxyurides. — The vaginal discharge may be found to contain 
both the adult oxyuris and its ova, either of which are readily 
detected under a two-thirds or a one-sixth objective (see Feces, page 
414). 

* "Phila. Co. Med. Soc./' Nov., 1901, p. 301. 



MENSTRUAL FLUID. 485 

MENSTRUAL FLUID, 

At the outset of menstruation the fluid is mucoid in character, 
but there is soon an admixture of red blood-cells until these cells 
so predominate that they determine the general characters of the 
fluid. With the decline of the flow the red cells decrease in number 
and the leukocytes make up the majority of the cellular elements 
found in the discharge. Large numbers of prismatic epithelial 
cells, showing areas of fatty degeneration and quantities of fatty 
debris, are also found at this stage of menstruation. 

Abortion. — Chorionic villi are expelled with the blood-clots 
after an abortion. They are to be recognized by their club-shaped 
extremities and by their epithelial covering. It is also possible in 
certain instances to recover decidual cells which are of large size 
and may assume polygonal, spindle-shaped, or imperfectly rounded 
forms. The nuclei of these cells are especially conspicuous on 
account of their irregular contour and large size. 

Lochia. — During the first twenty-four hours following de- 
livery the lochia are red (lochia rubra) and present the charac- 
teristic odor of blood. The discharge is composed of mucus, 
red blood-cells, leukocytes, and vaginal epithelium. During the 
second and third days the numbers of red corpuscles lessen 
greatly, while the leukocytes are increased in number, and this 
increase continues day by day until the secretion becomes grayish 
or white in color. 

From the tenth to the twelfth day the discharge becomes 
thicker, presents a mucoid appearance, is of a yellowish-white or 
milk-white color, and contains bacteria, among which strepto- 
cocci and staphylococci are found. It is to be borne in mind 
that the bacteria found in the discharge at this time are, as a rule, 
slightly, if at all, pathogenic. 

Membranes. — The retention of fetal membranes or the intro- 
duction of pathogenic bacteria into the birth-canal may cause a 
lessening or, at times, an absence of the lochia. This temporary 
decrease is followed by an excessive flow, which in some instances 
emits a decidedly fetid odor. Portions of fetal membranes or of 
placental tissue are often discharged with such lochia. 

Vulvitis and Vaginitis. — In inflammations of the vulva and 
vagina there is a marked increase in the secretion, which is com- 
posed principally of leukocytes and epithelial ceUs. Variations 
in the character of these cells are observed, depending upon the 
portion of the mucous surface from which they are derived. Red 
blood-cells are also present when the inflammation is intense. 
Rarely, indeed, do we find large shreds of desquamated epithelium 



486 SECRETION OF THE GENITAL ORGANS. 

that have sloughed from the vaginal wall, and casts of the vagina 
have been observed. When ulceration occurs and even in some 
cases of non-ulcerative vaginitis, a variable amount of pus is pres- 
ent. Vaginovesical or vaginorectal fistulae may permit the escape 
of the contents of the bladder or of the rectum into the vagina. 

Pruritus Vulvae. — Sehgmann * states that in chronic pruritus 
vulvae he has found a diplococcus constantly present ; and that the 
number of diplococci found are in direct proportion to the 
degree of activity of the pruritus. Seligmann's diplococcus closely 
resembles the gonococcus, differing from this organism in that 
it stains by Gram's method and that it possesses decided cultural 
characteristics (see Gonococcus, page 494). The diplococcus 
present in pruritus vulvae is destroyed by a 10 per cent, solution of 
guaiacol-vasogen. 

Membranous Dysmenorrhea. — During seizures of dys- 
menorrhea the vaginal secretion is found to contain, in addition 
to blood, many shreds of desquamated mucous membrane, and I 
have seen a complete cast of the uterine cavity. Portions of this 
membrane, when teased, show blood-cells, epithelial cells, and 
debris. A far more satisfactory method of study is to treat this 
membrane by employing the ordinary methods for examining 
pathologic tissues. 

Vaginal Blennorrhea. — The vaginal secretion is increased 
during sexual excitement, coitus, for some hours before the estab- 
lishment of and during the menstrual period, and during the 
latter months of gestation, at which time a profuse creamy dis- 
charge may be physiologic. 

Mycosis. — An increased vaginal secretion may result from a 
catarrhal process or it may be due in part to the existence of small 
mycotic areas situated near the orifice of the canal. Scrapings 
from these mycotic patches will be found to contain a profusion 
of bacteria and of fungi. Vaginal blennorrhea of gonorrheal 
origin has not been considered under this caption. 

Fungi. — The thrush fungus is rarely found in the vaginal 
secretions. 

* "Deut. med. Woch.," Feb. 22, 1902. 



CHAPTER X. 
TRANSUDATES AND EXUDATES. 

Fluid may be effused into the serous cavities of the body as the 
result of circulatory embarrassment (transudates) or of inflamma- 
tory processes (exudates). During health these serous cavities of 
the body contain quantities of fluid too small for analytic analysis. 
During pathologic processes, on the other hand, fluid may accumu- 
late in any of the serous sacs, as well as in the areolar connettive 
tissues immediately beneath the skin and between the muscles. 
When such conditions are the result of circulatory disturbances 
there is a deficiency in the ehmination of water by the kidneys 
and the retained fluid collects in the serous sacs as transudates. 
As a result of inflammatory processes of the serous membrane 
there is a similar accumulation of fluid in the serous sacs, and 
such collections are known as exudates. These two conditions, 
while they are widely different in origin, often give rise to the same 
clinical manifestation, so that at times it is difficult to decide to 
which class a given fluid belongs. Again, from clinical evidence 
alone, ovarian cysts, hydatid cysts, and cystic kidneys are liable 
to be confused with ascites. In such a case chemic analysis of 
the fluid may be the only means of deciding the diagnosis. 



TRANSUDATES. 

Transudates are, as a rule, serous in character and of a straw 
color. At times, however, they may assume a sanguineous ap- 
pearance from the admixture of blood, and in rare instances they 
are chylous. Transudates from the peritoneal cavity are usu- 
ally of low specific gravity, ranging between 1.005 and 1.015, 
which is somewhat lower than that of the exudate. Pleural transu- 
dates the result of cardiac disease or cirrhosis of the liver usually 
are below 1.012 in specific gravity, although in some instances they 
may reach 1.015. Pleural effusions due to inflammatory processes 
alone usually have a specific gravity between 1.018 and 1.030. This 
range of specific gravity includes that of those effusions composed 
of pus. This variation in the specific gravity probablv depends 

487 



TRANSUDATES AND EXUDATES. 

largely upon the albumins present in the fluid. Uric acid, a com- 
mon constituent of both transudates and exudates, is most abundant 
where the specific gravity is high. This uric acid is derived from 
the nuclein of the corpuscles. The nitrogen and proteid materials 
likewise influence the specific gravity. Serum-albumin and serum- 
globulin may be detected in either an exudate or a transudate; 
in the former they may constitute from 3 to 5 per cent, of the 
fluid; while in the latter they usually constitute between 0.5 and 
2.5 per cent, of the fluid. Ruess gives the following table: 

Specific Per cent, of Specific Per cent, of 

Gravity. Albumin. Gravity. Albumin. 

1.008 0.2 1.019 4.3 

i.oog 0.6 1.020 4.7 

i.oio i.o 1. 021 5.1 

i.oir 1.3 I.C22 5.5 

1.012 1.7 1-023 5-8 

1.013 2.1 1.024 6.2 

1.014 2.5 1-025 6.6 

1.015 2.8 1.026 7.0 

i-oi6 3.2 1.027 7.3 

1.017 3.6 1.028 7.7 

1.018 4.0 

Transudates, when allowed to stand for a time, do not coagulate 
spontaneously, except when there is an admixture of blood — a 
feature which often serves to distinguish them from exudates. 
Exhaustive chemic analyses of transudates have been made by 
Hoppe-Seyler and Hammarsten. 



MICROSCOPIC STUDY. 

In the microscopic study of transudates, exudates, cystic fluid, 
and even mucopurulent exudates the first step necessary is that 
the fluid be collected in the proper manner; secondly, that its 
cellular elements be thrown down in the form of a sediment ; and 
lastly, the further study of such sediments. 

Collection. — Whenever practicable, fluid should be collected 
by aspirating the sacs in which it is contained, then permitting 
it to flow into a sterihzed glass bottle or into test-tubes. In col- 
lecting fluid from the pleura it is always necessary to employ the 
special apparatus for this purpose; after which it is well to transfer 
some of the fluid to sterile test-tubes. Cystic and abdominal 
fluid may be allowed to flow directly into the test-tubes when 
collected after the method outhned under aspiration of the menin- 
ges or abdominal cavity, the same precautions being observed 
to prevent contamination of the fluid. Whenever it is possible, 
permit a portion of the fluid to flow directly into test-tubes con- 
taining cuhure-medium (see Meningeal Fluid, page 501). 



MICROSCOPIC STUDY. 489 

Caution. — Far more clinical evidence is to be obtained 
through cultural and inoculation studies than from a mere micro- 
scopic study of either transudates or exudates. Fluid, whenever 
obtained from a serous cavity, should in addition to being placed 
in steriHzed tubes be kept at a temperature of 37° C. (98.6° F.). 
Again, cultures should be made within a few hours after the fluid 
is removed from the body. 

Sedimentation. — Fluids, either serous or other, in which 
there are but few cellular elements, are best studied by permitting 
them to stand for a few hours in order that a precipitate forms, 
and in case this be copious, further sedimenting is not required. 
The precipitate that has collected at the bottom of the fluid, when 
but slight, should be Hfted by means of a pipet, and such sedi- 
ments placed in a tube of the centrifuge. Transfer all the sedi- 
ments from the receptacle to the tube, and then add sufficient 
of the liquid portion of the exudate to fill the tube; place in the 
machine and centrifugalize for from three to ten minutes, or until 
an appreciable amount of sediment has collected at the bottom of 
the tube. 

Lift the sediment from the bottom of the tube into a small 
pipet, and place a small drop of the thickest of this upon the 
center of a clean slide. Smear this drop thinly over the slide by 
using a second slide (see Method of Making Blood Smears, page 
35), and permit to dry in the air. 

Fixing. — My experience has been that the best results are to 
be obtained by placing such films of the sediment upon a heated 
copper plate and permitting them to remain at the proper temper- 
ature — point where the water boils when dropped upon the plate 
— for from one-half to one hour (see Fixing oj Blood, page 74). 
Fairly good results are to be obtained, however, by placing the 
slide in a sHde-forceps and passing it directly through the flame 
several times. It is necessary to keep the slide as hot as it can 
be borne to touch the palmar surface of the hand for at least 
three minutes. Whenever feasible, the former method is to be 
employed. 

Staining. — At least one specimen film from the sediment of 
every fluid should be stained for the tubercle bacillus (see Sputum, 
page 438). Stain a second with anilin-gentian- violet and continue 
with Gram's method (see Gonococcus, page 494). It is my custom 
to stain a third slide with an alcoholic solution of eosin for one-half 
minute and Delafield's hematoxylin for three minutes; and one 
slide with a saturated alcoholic solution of sudan III for from 
one to three minutes for the detection of fats which are stained 
a pink with this reagent; a knowledge of the presence of fats is 



490 TRANSUDATES AND EXUDATES. 

also gained by staining with a solution of osmic acid, which stains 
such substances black. The eosin is employed for the detection of 
cells showing eosinophihc granules, such leukocytes being rather 
common in pleural and peritoneal fluids. 

Cytodiagnosis consists in a differential study of the cellular 
elements found in such fluids. An excess of lymphocytes is probably 
suggestive of tuberculosis; while a preponderance of polynuclear 
cells points toward suppurative processes. In transudates, endo- 
thehal cells are found in sheets and clusters. In cancerous in- 
volvement of the serous surfaces one would expect to find many 
endothelial cells in the effusion from involved sacs. 

Transuded fluid will be found to contain a few leukocytes 
and endothelial cells, many of which show evidence of fatty degen- 
eration. In ascitic fluid during the course of myelogenous 
leukemia many eosinophils and mast-cells have been noted. 
In cases in which the fluid is concealed for a long time crystals of 
cholesterin and Charcot-Leyden crystals may be found, the former 
being usually found in hydrocele fluids. 

Renal Cysts. — The fluid of hydronephrosis is readily distin- 
guished from transudate fluid by both chemic and microscopic 
study. The specimen should be examined at once for urea, and 
if that substance is present in large quantity, an opinion as to its 
renal origin can be formed. While the presence of urea would 
serve to distinguish between the fluid from a renal cyst and ascites, 
it does not serve the same purpose in case the diagnosis lies be- 
tween an ovarian cyst and a cyst of the kidney. Urea is at times 
present in the fluid of the former in fairly large amounts. Uric 
acid is present in the fluid of a kidney cyst, but it may too be found 
(traces) in the fluid from an ovarian cyst. The presence of 
epithelial cells from the uriniferous tubules is regarded by some 
authors as distinctive, but personally I should hesitate to make 
a diagnosis upon such a finding. 

Ovarian Cyst. — The general appearance of fluid from ovarian 
cysts is very inconstant, but there is one feature which serves to 
distinguish it from the fluid of the majority of cysts — its high 
specific gravity. This is usually above 1.020, 1.023 ^o 1.025 
being quite common, although I have seen such a fluid with a 
specific gravity of i.oio. The fluid from an ovarian cyst shows 
no tendency to coagulate and is of an alkaline reaction. 

The large quantity of tissue debris present is rather charac- 
teristic of the fluid from ovarian cysts, although this finding is by 
no means reliable. If a hemorrhage has occurred within the cyst, 
the general findings are materially altered, and the fluid may be 
bloody or it may present a chocolate color. The cellular elements 



MICROSCOPIC STUDY. 49 1 

also may be distorted, and at times colloid-like bodies have been 
detected in the sediment. These colloid-like bodies are said to 
be found in connection with colloid cysts; but microscopic exami- 
nation of the fluid is not of itself a reliable means of determining 
the variety of the cyst. The fluid from an ovarian cyst will be 
found to contain, in addition to the elements just named, hair, 
crystals of hematoidin, fat, and cholesterin. Chemically the fluid 
from ovarian cysts contains a variable amount of albumin and 
metalbumin. 

Metalbumin Test. — Place lo c.c. of cystic fluid in a test-tube 
and add 30 c.c. of alcohol; shake well and allow to stand for 
twenty-four hours; filter, squeeze out the precipitate, and suspend 
it in water; filter again. The second filtrate is opalescent, becomes 
turbid on boiling, but does not form a distinct precipitate. Acetic 
acid does not induce a precipitate, while acetic acid and potassium 
ferrocyanid produce a thick yellowish fluid. Millon's reagent 
gives a bluish-red color (see page 217). Concentrated sulphuric 
acid produces a violet color, as does glacial acetic acid. According 
to Huppert, when the fluid contains metalbumin, it yields a re- 
ducing substance when boiled with sulphuric acid. Metalbumin 
is also a constituent of other pathologic fluids. 

Hydatid Cysts. — Fluid obtained by paracentesis from a hyda- 
tid cyst is, as a rule, clear and of an alkaline reaction, and has a 
specific gravity of 1.004 to i.oio. Such fluid often contains a 
small amount of grape-sugar and of albumin, and a larger amount 
of inorganic salts. Inosite and succinic acid are occasionally 
formed. 

Hooklets. — The characteristic clinical features of the fluid 
from a hydatid cyst are the hooklets, the scolices, and the shreds 
of faintly yellow membrane (Figs. 122-125). The inner surface 
of this membrane is faintly granular and shows transverse stria- 
tions. The individual scolex is best described by the illustrations, 
as are also the echinococcic hooklets. It is to be borne in mind 
that a positive diagnosis of hydatid disease is attained only 
through the detection of these elements. 

Pancreatic Cysts. — The fluid from a pancreatic cyst is usually 
bloody. It varies in specific gravity from i.oio to 1.030. Alethe- 
moglobin and crystals of cholesterin are often present. The chief 
proteid is serum-albumin. Pancreatic cyst-fluid contains a dia- 
static ferment, though this is not a feature characteristic of the 
pancreatic juice. The presence of the reactions for maltose in 
a fluid obtained by abdominal puncture is always strongly sug- 
gestive of cystic disease of the pancreas. 

Fistulous Secretions. — The secretion from anv abnormal 



492 TRANSUDATES AND EXUDATES. 

channel varies with the viscus or the set of glands that the fistula 
drains. In analyzing such secretions it is necessary to examine 
them for the various bodv-fluids. 



EXUDATES. 

An exudate may be serous, seropurulent, chylous, purulent, 
hemorrhagic, or putrid. 



SEROUS EXUDATES. 

Exudates composed for the most part of serum are clear, pale, 
or of a light strav^ color, and display a specific gravity not greater 
than 1.008. See Specific Gravity oj Transudates, p. 488. When 
serous exudates are permitted to stand, they develop a whitish 
color and more or less fibrinous coagula. 

Microscopically such exudates may contain few red corpus- 
cles, polynuclear leukocytes, and when derived from the serous 
sacs, endothelial cells showing areas of fatty degeneration are to 
be found. 

Generally speaking, exudates display a higher specific gravity 
than the transudates, and when there has been added to a serous 
exudate a variable amount of fibrinous material, the exudate is 
referred to as serofibrinous in character. 

Inoscopy. — This method for the study of inflammatory 
exudates recovered from the serous sacs has recently been de- 
scribed by A. Jousset, and consists in the digestion of the fibrinous 
coagula of such fluids with the following fluid: 

Pepsin 2 gm. 

Glycerin 10 c.c. 

Hydrochloric acid lo c.c. 

Sodium fluorid 3 gm. 

Distilled water 1000 c.c. 

The digested coagulum is now sedimented, and such sediment 
stained and examined for tubercle bacilli. Jousset used the sedi- 
ment for the inoculation of animals. It is claimed for inoscopy 
that the exudate thus treated is more likely to excite tuberculosis 
when injected into animals than is the fresh sediment from such 
exudates. 

SEROPURULENT EXUDATES. 

The term seropurulent is employed to designate an exudate 
in which there has been the admixture of a moderate number of 
leukocytes and pus-cells. 



PURULENT EXUDATIONS. 493 

CHYLOUS EXUDATES. 

Exudates of chylous and chyloid fluids are to be found in the 
serous sacs, most frequently in the peritoneal cavity, and less 
commonly in the pleural cavities; they have been found in the 
pericardium. Chylous exudates, like other exudates, will be found 
to contain sugar, and, as a rule, more than a mere trace is to be 
detected. 

Characteristics. — These exudates are of a milky appearance. 
When they are chyloid, they bear a close resemblance to pus. 
The decided turbidity of these fluids is due to the presence of 
fat-globules, as is shown by microscopic examination. I have 
studied two cases of chylous fluid obtained from the peritoneum 
in which no chyle was present.* It has been shown by various 
observers (Lion) that in chyloid fluids the turbidity depends upon 
the presence of albuminous substances (nucleo-albumins), and 
degenerated epithelial cells may account in part for the turbidity 
of chylous exudates. 

For distinctive features aind Clinical Significance of Chylous 
Exudates, see p. 537. 

HEMORRHAGIC EXUDATES. 

A hemorrhagic exudate is essentially serofibrinous; it differs 
from that commonly known as serous exudate only by the ad- 
mixture of red blood-cells. Microscopically, such an exudate 
will be found to contain a profusion of red blood-cells, poly- 
morphonuclear leukocytes, a few endothelial cells, and cholesterin 
crystals. Hemorrhagic exudates collect in the pleurse and in the 
peritoneal cavity as a result of tuberculosis, carcinoma, sarcoma, 
and cirrhosis of the liver. (See Cytodiagnosis, page 534.) 



PURULENT EXUDATIONS. 

Pus is a turbid fluid of a grayish-white or greenish-yellow color 
and of an alkaline reaction. It varies greatly in its consistence 
and specific gravity. When spoken of as an exudate, we mean 
that pus has accumulated in one of the natural cavities of the body. 
Occasionally we refer to an effusion of pus in the tissues (phleg- 
mon) ; and at times to pus secreted from the free surface of a wound 
as an exudate. 

When collected in a conic glass and allowed to stand in a cool 

* " Journ. Amer. Med. Ass.," Feb. 18, 1905. 



494 TRANSUDATES AND EXUDATES. 

place, pus separates into two layers — the upper layer is of a light- 
yellow color and of a watery consistence, while the lower layer is 
creamy, opaque, and contains the pus-cells. The admixture of 
blood or its pigment may give a brownish or brownish-red color 
to the latter layer. Putrid pus is, as a rule, liquid, of a greenish 
or brownish-red color, and emits a decided odor of indol and 
skatol. 

Microscopic Study. — When examined under the microscope, 
pus may be found to contain crystals of cholesterin, hematoidin, 
crystals of fatty acids, degenerated leukocytes, giant pus-corpuscles, 
pus-cells showing deposits of fat, red blood-cells, and debris. 
Pus thinly smeared upon a slide, fixed by heat, and stained with 
the ordinary anihn dyes will be found to contain bacteria in the 
majority of instances, but occasionally bacteria-free pus is to be 
encountered. 

Staining. — At least one slide from all specimens of pus should 
be stained for the tubercle bacillus. Stain for twenty-four hours 
with a w^eak solution of carbolfuchsin (see Sputum, page 438), 
since this organism commonly figures in the production of sup- 
purative maladies. Although it is questionable whether or not 
the tubercle bacillus of itself is capable of inducing suppuration, 
experience shows that it is often associated with the pus- 
producing organisms. Bacteria-free pus, when obtained from a 
serous cavity, should be diluted, say, ten to twenty times, with 
sterile water, and a small quantity of the mixture injected into 
the peritoneum of either a rabbit or a guinea-pig. In this way 
it is at times possible to establish a positive diagnosis when the 
microscope has failed to detect the tubercle bacillus. 

Gonorrhea. — Inflammatory processes of the male urethra 
are, as a rule, of bacterial origin. The gonococcus is usually 
the pioneer infecting organism, which by its development reduces 
the resisting power normally present in the urethral mucosa, thus 
rendering this surface more susceptible to the development of 
other pathogenic bacteria. 

A few drops of a serous exudate may escape from the meatus 
before the characteristic creamy discharge of gonorrhea is ob- 
served. It is possible to make a diagnosis of gonorrhea in its 
earliest manifestation by examining cover-glass preparations of 
this initial serous discharge. 

Microscopic Study. — Direct the patient not to void urine 
for one or more hours before he presents himself for examination. 
When he is seen, have him pull back his prepuce; place the finger 
between his testicles, and then gradually draw it forward. By 
this means pus will escape from the meatus. Touch this drop 



PLATE 34. 




1. Urethral pus stained by Gram's method; note gonococci stained brown and 
situated in pus-cells and epithelial cells; staphylococci and streptococci stain 
violet (obj. B. and L. one-twelfth oil-immersion). 

2. Urethral pus containing gonococci and stained by Small's method (obj. B. 
and L. one-twelfth oil-immersion). 



PURULENT EXUDATIONS. 495 

of pus with a tooth-pick or with the edge of a sHde (see Method 
oj Making Smears, page 35), and smear it thinly over nearly 
the entire length of a microscope shde. Fix by passing it through 
the flame, care being taken lest too great a heat be apphed. 

The specimen is now ready for staining the gonococci, all 
of which stain readily by any of the anilin dyes. Eosinophilic 
leukocytes are often present in gonorrheal pus, but they bear no 
fixed proportion to the number of such cells found in the blood. 
The percentage of eosinophihc cells in the pus, however, is not 
in excess of the percentage found in the blood (see Cytodiagnosis, 
page 490). Gonococci are seldom found within the eosinophilic 
cells. Mast-cells are unusual. 

For practical laboratory work I have adopted the method 
devised by my assistant. Dr. J. Hamilton Small, and I have found 
that this plan of staining gives as satisfactory results as the other 
more compHcated methods. 

SmalVs Method. — After the pus has been smeared and fixed 
in the usual manner, proceed as follows: 

1. Place in a slide-forceps and stain for thirty seconds with 
a 2 per cent, aqueous solution of methylene-blue. 

2. Wash in a 10 per cent, solution of sodium hydroxid. 

3. Pour off the sodium-hydroxid solution and immediately 
follow with carbolfuchsin (dilution i-io), and allow to stain for 
fifteen seconds. 

4. Wash in water, dry, and mxount. 

By this method the general field will be stained pink; the 
nuclei of the leukocytes, pus-cells, and epithelial cells are stained 
a dark blue. The gonococcus stains a brilhant blue (Plate 34), 
while other pus-producing bacteria stain a less intense blue. 

Methylene-blue. — Add to the specimen a few drops of an 
aqueous solution of methylene-blue (2 per cent.), and allow to 
stain for from two to three minutes without the addition of heat. 
By this method the gonococcus will be found to stain a deep 
blue, while the pus-cells and the epithehal cells are less intensely 
stained. Other bacteria, such as the staphylococcus and the 
streptococcus, when present, are also stained, but the staphylo- 
coccus is seldom arranged within the bodies of the pus-cells 
and is, therefore, readily differentiated from the gonococcus. 
By this stain it is not possible to distinguish the gonococcus 
from other cocci by its peculiar diplococcus (biscuit) formation. 

Gramas Method. — i. To a fixed specimen of urethral pus 
add a few drops of anihn-gentian- violet ; heat to steaming, and 
allow to stain for fifteen seconds. 

2. Wash in water, and without drying — 



496 TRANSUDATES AND EXUDATES. 

3. Add a few drops of Gram's iodin solution and permit to 
remain for from one to two minutes. 

4. Wash the specimen in 70 per cent, alcohol until but a 
faint violet color remains. 

5. Stain for tw^o minutes with a saturated alcohohc solution 
of Bismarck-brown. Wash in water, dry in the air or by heating 
gently, mount in Canada balsam, and examine under an oil- 
immersion objective. 

By Gram's method the gentian- violet stains all bacteria pres- 
ent, but after treatment with Gram's solution of iodin and alcohol 
the gonococcus is decolorized, while streptococci, staphylococci, 
and other diplococci remain violet. The addition of a second 
stain — Bismarck-brown — stains the previously decolorized gono- 
coccus. Thus, by this method, the gonococcus is stained a hght 
brown, while other pathogenic bacteria are stained violet. The 
nuclei of the pus-cells and of the epithelial cells stain a mahogany 
color, while the bodies of these cells stain a less intense brown. 

Streptococci. — In a few instances I have been able to study 
urethral pus in which the general symptoms resembled those of 
gonorrhea, except that the urethritis subsided in a shorter time, 
and in which streptococci only were present. In a case studied 
at the Medico- Chirurgical Clinic, through the courtesy of Dr. 
Leon Gans, I was able to obtain streptococci only from both 
scrapings and cultures made from a small cervical ulcer from the 
woman with whom the patient had been cohabiting. Careful 
cultural studies of the streptococcus obtained from the cervix and 
that obtained from the urethral pus of the man showed these 
organisms to be practically identical. Furthermore, inoculations 
showed them to be highly pathogenic for animals. This patient 
finally developed orchitis involving both testicles. 

Streptococci and staphylococci appear in the urethral discharge 
during acute gonorrhea coincidentally with improvement of the 
symptoms. In fact, I have grown to regard the appearance 
of the streptococcus as a precursor of the disappearance of the 
gonococcus from the urethral pus. Indeed, it is rare to find 
gonococci when the pus contains many other bacteria. One 
often sees specimens of urethral pus from cases of chronic ure- 
thritis in which streptococci, staphylococci, extracellular diplo- 
cocci, bacilli, and diplobacilli are to be found in great numbers. 
Occasionally, in such specimens, extracellular diplococci may be 
found, the staining reaction of which, by Gram's method, is 
characteristic of the gonococcus. In my experience these organ- 
isms have not proved to be gonococci, and I do not recall ever 
having found gonococci when the above-named organisms were 
numerous. 



PURULENT EXUDATIONS. 



497 



Urine. — It is impracticable to search for the gonococcus in 
urinary sediments. My experience differs widely from that of 
many writers, since I have been unable to recover the gonococcus 
from this source, even though the urinary sediments contained 
considerable urethral pus, and although the pus collected from 
the urethra showed many gonococci. 

Glanders. — In the cutaneous form of glanders pus collected 
from the abscesses will be found to contain bacilli known to 
this disease. The Bacillus mallei may also be recovered from 
the nasal secretions and from the blood. 

Anthrax. — Pus collected from the abscesses and serum from 
the vesicles of anthrax commonly contain many large segmented 
bacilh (Fig. 207). These 
bacilh are readily stained by 
the anihn dyes, so that their 
detection is most simple. 

Tetanus. — The exudate 
from the initial wound of 
tetanus is often found to con- 
tain many bacilli clubbed at 
one extremity. 

Detection. — Secure scrap- 
ings from the wound or from 
the tissues immediately sur- 
rounding the site of the initial 
puncture, smear these scrap- 
ings thinly upon a cover-glass, 
fix by heat, and stain for from 
one to two minutes with a 

solution of carbolfuchsin, or with a 2 per cent, aqueous solution 
of methylene-blue. 

Leprosy. — Lepra bacilli are often to be found in the exudates 
from suppurative surfaces. They are also to be detected by 
incising a small lepra tubercle, compressing it firmly, and smear- 
ing the exudate upon a slide (see Staining oj Tubercle Bacillus, 
page 438). 

Animal Parasites.— The Amoeba coH (page 388), Balantidi- 
um xoH (page 395), and certain protozoa may be encountered in 
purulent exudates. 

Filaria. — The Filaria sanguinis hominis may collect in the tissues 
and produce a large chylous exudate which in time makes its way 
to the surface and appears not unlike an abscess (see Guinea-worm, 
page 149). Living filaria are occasionally found in this exudate. 
The echinococcus (page 404) and Schistosoma hamiatobium (page 
32 




Fig. 207. — Bacillus of anthrax in blood of sub- 
ject who died of the disease (Jakob). 



498 



TRANSUDATES AND EXUDATES. 




295J are occasionally seen in abscesses of the liver, lungs, etc., and 
have already been discussed at length. The trypanosoma may 

also be found in the exudate 
recovered from ulceratinsr sur- 

o 

faces (see Trypanosomiasis, 
page 151). 

Micrococci. — P u s from 
whatever source is hkely to 
contain cocci, among which the 
Streptococcus pyogenes (Fig. 
2o8j, the Staphylococcus pyo- 
genes (Fig. 209), the pneumo- 
coccus, the Diplococcus intra- 
cellularis (meningococcus) (Fig. 
213), the gonococcus, and the 
Micrococcus tetragenus are the 

Fig. 208.— Streptococcus pyogenes from moSt COmmon. The BaciUuS 
a case of empvema secondars- to pneumonia , t-> -n t 

(Jakob). ' ' pyocyaneus, the Bacillus coli 

communis, the bacillus of Fried- 
lander, are also frequently found in pus. and it is the rule to find 
many other bacteria in purulent exudates, the characteristics of 
which it is not necessary to discuss at length. ( For the methods 
for the determination of questionable organisms recovered from 
pus the reader is referred to 
special works on the subject of 
bacteriology.) 

Fungi. — Pus resulting from 
the development of the actino- 
myces (Fig. 183) is occasionally 
to be recovered from abscesses 
in various portions of the body. 
These abscesses develop most 
often in the structures adjacent 
to the buccal cavity, and have 
also been described in relation 
with the genito-urinary tract and 
the serous surfaces. Van der 
Veer regards thoracic, pulmon- 
ary, and abdominal actinomy- 
cosis as being a common occur- 
rence, and pus from the thoracic and abdominal regions should 
always be examined for the actinomyces. Cutaneous lesions have 
occasionally been observed. A. Poncet has reported in detail 
146 cases of actinomvcosis hominis collected from the various 




Fig. 209. — Staphylococcus pyogenes arous 
from an abscess of the parotid gland (Ja- 
kob i. 



PURULENT EXUDATIONS. 499 

portions of France. Erving * reports six cases, and in addition 
reviews the literature on American actinomycosis. 

Detection. — Pus from the lesions of actinomycosis usually 
contains small kernels or nodules. Place one of these nodules 
upon a slide and crush it by pressure applied to a heavy cover- 
glass or a second slide; then examine the specimen (unstained) 
under a one-fourth or a one-sixth objective for the presence of the 
ray-like formation of the fungus (Fig. 183). Actinomycotic pus 
may be free from bacteria, although the finding of cocci and 
bacilli in such pus should not discourage a careful search for 
the actinomyces. 

This fungus may be cultivated upon the ordinary culture- 
media at incubating temperature, yet in the majority of instances 
cultural studies are not required. During my service at the 
Philadelphia Hospital (1904) I studied a case in v^hose sputum 
the actinomyces was first found by my colleague, Dr. Rosenberger. 

* "Johns Hopkins Hosp. BuL," Nov., 1902, p. 261. 



CHAPTER XI. 



CEREBROSPINAL FLUID AND SYNOVIAL FLUID. 



CEREBROSPINAL FLUID. 

The study of the cerebrospinal fluid often furnishes valuable 
information in connection with both cerebrospinal affections and 
in differentiating meningitis from other conditions closely re- 
sembling it. This fluid may contain animal parasites (see Try- 
panosomiasis, page 151). 

Collection of the Fluid. — After the age at which the cranial 

bones have united lumbar puncture 
becomes necessary in order to with- 
draw the cerebrospinal fluid; but 
early in life a needle may be thrust 
through the anterior fontanel and 
fluid withdrawn from the lateral 
ventricles. 

Lumbar Puncture. — Place the 
patient upon his side, flex the supe- 
rior thigh upon the abdomen, and 
then cleanse and render the skin 
of the lower thoracic and lumbar 
regions aseptic. The site of punc- 
ture should be on a level with the 
junction of the third and fourth 
lumbar vertebras at a point one- 
half inch to the right or left, above 
the media?i line, depending upon 
which side the patient is lying (Figs. 
210, 211, 212). Anesthetize the skin 
by spraying with ether. Select a 
small needle, from four to six inches 
in length, with which to make the 
puncture, since it is often more 
than three inches from the surface of the skin to the spinal canal. 
Place the index-finger firmly upon the needle, as a guide to the depth 

500 




Fig. 210. — Anatomic preparation 
from a child twenty-one months old, 
showing location for lumbar puncture 
between third and fourth spinous pro- 
cesses (Friihwald). 



CEREBROSPINAL FLUID. 



501 



of the puncture, and thrust it obhquely through the tissues at such 
an angle that the point of the needle will pass between the laminae of 
the vertebras. It is not necessary to attach a syringe to the needle, 




Fig. 211.— Method of inserting needle in lumbar puncture — child in lying posture. 




Fig. 212. — Method of introducing needle in lumbar puncture — child in sitting posture. 



because the spinal fluid will escape as soon as the needle enters 
the cerebrosubarachnoid space. 

Allow a few drops of the fluid to flow directly into a sterile 



502 



CEREBROSPINAL FLUID AND SYNOVIAL FLUID. 



test-tube. This tube is then corked and placed in an incu- 
bator at a temperature of 37° C. (98.6° F.). It is well to make 
cultures from this fluid upon LofHer's blood-serum, bouillon, agar- 
agar, and glycerin-agar. The tubercle bacillus when present will 
develop upon the glycerin-agar within from ten days to two weeks. 
The Diplococcus intracellularis, the pneumococcus, and the 
other pathogenic organisms will be found to develop appreciable 
growths in from twenty-four to forty-eight hours when kept at 
37° C. (98.6° F.). 

As the fluid continues to flow drop by drop it should be col- 
lected upon several clean slides, dried in the air, fixed by heat, 
and stained. (See Cytologic Study, p. 538.) 

Staining. — Cerebrospinal fluid should always be stained 
for the tubercle bacillus (see page 438) by Gram's method 

for the detection of the 
Diplococcus intracellu- 
laris, and also to determine 
whether or not certain ba- 
cilli present are decolor- 
ized through this method 
of staining (the bacillus 
of Friedlander and the 
colon bacillus decolorize). 
Stain a third shde with a 
2 per cent, aqueous solu- 
tion of methylene-blue. 
The same routine should 
be followed in the stain- 
ing of bacteria cultivated 
from the cerebrospinal 
fluid. It is not within 
the scope of this volume 
to deal with the cultural 
characteristics of the dif- 
ferent bacteria known to invade the meninges, and for such knowl- 
edge the reader is referred to special works on bacteriology. Micro- 
scopically the normal cerebrospinal fluid will be seen to contain 
a few leukocytes and a small amount of granular matter; but 
when the fluid is purulent, it differs in no way from the pus found 
in any other of the serous sacs. 

Diplococcus Intracellularis.— This organism was first de- 
scribed by Weichselbaum, and later studied at length by Council- 
man and Mallory and Wright of this country. It is generally 
conceded to be the exciting cause of epidemic meningitis. The 




Fig. 213.— Diplococcus intracellularis. Menin- 
geal pus obtained by lumbar puncture from case of 
epidemic cerebrospinal fever observed at Phila- 
delphia Hospital (obj. Spencer one-twelfth oil-immer- 
sion). 



CEREBROSPINAL FLUID. 



503 



characteristic situation of this diplococcus is within the bodies 
of the pus-cells and the leukocytes, but many extracellular diplo- 
cocci are always present (Fig. 213). The situation of the cocci 
within the pus-cells and the fact that they are not stained by 
Gram's method are features displayed by the Diplococcus 
intracellularis and the gonococcus. The diplococcus of men- 
ingitis, however, grows readily upon the ordinary culture-media, 
and this serves to distinguish it from the gonococcus, which is 
grown upon a special medium only. 

Personally I have recovered from the meningeal exudate the 
Bacillus tuberculosis, the colon bacillus, the Streptococcus 
.pyogenes, the Staphylococcus pyogenes albus, the Staphylo- 
coccus pyogenes aureus, the pneumococcus, and the Diplococcus 
intracellularis meningitidis. Other observers have also found 
the Bacillus meningitidis 
purulenta and the typhoid 
bacillus.* In one case 
studied at the Philadel- 
phia Hospital in which 
meningitis followed puer- 
peral sepsis I recovered a 
capsulated bacillus from 
both the meninges and 
the uterine cavity at post- 
mortem. The bacilli from 
both sources were identical 
in every respect and were 
highly pathogenic for 
guinea-pigs. In many re- 
spects this organism re- 
sembled the bacillus of 
Friedlander, but I hesi- 
tate to regard it as that 
organism, since in certain 
cuhural studies it differed widely from the organism described 
by Friedlander. In a second case I recovered the Diplococcus 
intracellularis from the meninges antemortem and from the endo- 
cardium, the pericardium, and a myocardial abscess at post- 
mortem. Through the courtesy of Dr. J. H. Lloyd a case was 
studied in which the meningeal pus contained only colon bacilli. 

In my experience it has been rather common to find the diplo- 
coccus of pneumonia in association with the Diplococcus intra- 

*C. Straubli, "Deut, Archiv. f klin, Med.," Bd. Ixxxii, p. go. 




Fig. 214. — Meningeal pus containing colon bacilli. 
Observed at Philadelphia Hospital. Pus recovered 
at postmortem (obj. B. and L. one-twelfth oil-immer- 
sion). 



504 CEREBROSPINAL FLUID AND SYNOVIAL FLUID. 

cellularis; and when this condition exists, certain of the diplococci 
are not decolorized by Gram's method. 

Galdi and Appani* have found a large amount of uric acid 
in purulent cerebrospinal fluids. 

For cytologic study of spinal fluid see p. 538. 



SYNOVIAL FLUID, 

The study of the fluid from the serous sacs of the various 
articulations may provide valuable clinical knowledge in many 
instances, as is illustrated by the fact that when an arthritis is 
found to complicate either lobar pneumonia or gonorrhea, the 
specific diplococcus of these diseases may be recovered from the 
synovial fluid of the infected joints. The Diplococcus intra- 
cellularis is sometimes recovered from the synovial fluid, and 
the tubercle bacillus, which is known to invade these structures, 
may be found. Following traumatism and following lacerated 
or punctured wounds of the joint regions some one or more of the 
pus-producing organisms may be recovered from the synovial 
fluid and other bacteria may also be found. During the course 
of scarlet fever and of rheumatism bacteria may be recovered 
from the joint fluids of inflamed joints. Throughout England 
and America the belief is quite strong that acute articular rheu- 
matism is probably excited by a coccus — "micrococcus rheumat- 
icus." Beattie,t after a series of experiments, concludes that 
the "micrococcus rheumaticus" is a distinct microbe, and an 
etiologic factor in acute articular rheumatism. The researches 
of Cole, Jachmann, and of the author fail to confirm the findings 
of Beattie, since micrococci were not found in the fluid from in- 
fected joints or in the blood of persons suffering from acute articu- 
lar rheumatism. 

Collection. — The skin overlying the joint should be scrubbed 
well with water and green soap, and a wet mercury-bichlorid 
dressing should be applied for a few hours. It is my custom 
to wash the skin-surface over the joint with ether just before the 
puncture is made. Then determine that there is a distinct 
fluctuation over the joint, and, placing the finger about one-half 
inch from the point of a previously sterilized needle, plunge it 
quickly into the sac. The point of puncture should not be on a 
level with the articular surfaces of the bones, but at least one-half 
inch from the joint cavity, so as to avoid all possibihty of wound- 
ing the articular cartilages. 

* "Brit. Med. Journ.," Dec. 3, 1904 t "Riforma Med.," Dec. 14, 1904. 



SYNOVIAL FLUID. 505 

The technic for the making of cultures and cover-glass prepara- 
tions differs in no way from that described in the chapter devoted 
to the study of the cerebrospinal fluid (page 500). 

Cultures. — In certain chronic conditions in which there is 
an accumulation of fluid within the synovial sacs this fluid, when 
smeared thinly upon a slide and stained, will be found free from 
bacteria. When, however, from ten to thirty drops of such fluid 
are added to from 150 to 500 c.c. of bouillon and placed at an 
incubating temperature for forty- eight hours, a certain clouding 
of the bouillon is produced. Bouchard has described extremely 
minute organisms which develop from the fluid obtained from 
chronic rheumatic conditions. Through the courtesy of the late 
Dr. Frederic A. Packard I was privileged to repeat these in- 
vestigations during my term of service at the Pennsylvania Hospital. 
The clouding of the bouillon described by Bouchard was observed 
in every instance, but I was unable to detect, with any degree 
of satisfaction, the miniature cocci to which this author has re- 
ferred. I am, therefore, inclined to regard the change occurring 
in the bouillon as due to chemic changes rather than to bacterial 
development. 



CHAPTER XII. 
DISEASES OF THE SKIN. 

Favus. — Honey- combed ring- worm, or Tinea favosa, is occa- 
sionally encountered in this country and is known to be common 
throughout Europe. It usually affects the scalp and the eye- 
brows; but it may involve the face and other portions of the 
body. In one instance, studied at the Philadelphia Hospital, a 
case in which the patient's entire scalp and genitalia had been 
involved, I recovered the fungus from a mycotic patch on the 
tonsil. 

The disease is due to the infiltration of the epidermis and 
hair-follicles with the mycelium and spores of a fungus which 
is usually termed Achorion Schonleinii. This name, according 
to many observers, includes several species of the fungus. 
During the past three years five cases of favus have been treated 
at the dermatologic clinic of the Medico- Chirurgical Hospital. 
In all these cases the patients, who were of foreign birth, had 
probably contracted the disease before emigrating to this country. 

Collection. — Remove one of the crust-like masses, cut it in 
half, and from near its center chip out a small portion. Place 
this portion of the mass on the center of a slide, add a few drops 
of water, and crush the specimen completely. Now spread the 
fragments in a thin layer on the slide, fix by heat, and stain by 
heating for from one to two minutes with carbolfuchsin ; wash 
in water, dry, mount, and study under a one-sixth objective. 
The specimen will be found to consist almost entirely of granular 
debris, but in the thin portions of the field a few imperfectly 
formed, oval or partially rounded bodies may be seen, as well 
as ribbon-like segmented chains of the fungus. These ribbon- 
like particles (mycelia) may be the only finding, and in certain 
cases they will be seen to divide dichotomously; they always 
show distinct segmentation, and are surrounded by a fighter area 
within which the fungus stains deeply. They are well seen under 
an oil-immersion objective (Fig. 215). The fungus is stained less 
satisfactorily with methylene-blue and the other anilin dyes. 

A hair drawn from the infected area should be placed in a 
10 per cent, solution of sodium hydroxid for from one-half to 

506 



TINEA TONSURANS. 



507 



one hour, then placed on a shde, flooded with water, and covered 
with a cover-glass. By careful focus under a one-sixth 
objective it is at times possible to detect many threads and ap- 
parent spores of the fungus within the sheath of the hair-bulb. 
The infection of the hair is best demonstrated, however, by sec- 
tioning, and without such treatment I have found it difficult 
to demonstrate the presence of the fungus. Favus may, in 
rare instances, involve the stomach-walls, in which case this 
fungus may be found in the gastric secretion. 

Tinea Tonsurans. — Tinea tonsurans is one of the most 
common of skin conditions in which clinical laboratory methods 




Fig. 215. — Tinea favosa, showing threads of the fungus ; crusts from scalp of patient observed 
at Philadelphia Hospital (obj. B. and L. one-twelfth oil-immersion). 



are of great service. The exciting cause is a small-spored fungus, 
Trichophyton microsporon or Microsporon Audouini. 

Detection. — Remove one of the diseased hairs, which will 
usually be found to vary from one-eighth to one-fourth of an inch in 
length, place the hair-stump and root in a solution of liquor 
potassae, and allow to soak for one hour. Place the hair on a 
shde, flood it with water, and examine under a one-sixth or a 
one- eighth objective. The hair will be seen to be ensheathed by 
round bodies, which vary from 2 to 3 />< in diameter. These bodies 
are closely packed together, but by gently pressing a cover-glass 
on the hair they may be separated slightly; by rupturing the 
sheath, spores may be forced outside of the hair. Prolonged 



5o8 



DISEASES OF THE SKIN. 




Fig. 216. 



-Epidermic scales from a case of squamoiis herpes tonsurans; 
hydroxid preparation; magnified 275 times (EichhorstJ, 



potassium- 



'-Jf 







LTi. 



I 2 3 

Fig. 217. — TriclTophyton tonsurans (megalosporon) : i. An endothrix ; 2, microsporon 
(one-half hair-shafl) itrom case of several years' standing), scrapings from surface of diseased 
area ; 3, an ectothrix (trom Kerion). 



TINEA BARB^. 



509 



soaking of the hair in hquor potassae will enable one, by careful 
focusing, to detect mycelia surrounding the sheath (Fig. 217). 

Tinea Trichophyton Endothrix. — The spores and mycelia 
of Tinea trichophyton endothrix (Fig. 217), as well as of Megalo- 
sporon endothrix and Megalosporon ectothrix (Fig. 217), may be 
detected in the manner described under Tinea tonsurans. A very 
small percentage of cases of ring- worm are caused by the latter of 
these parasites, and the fungus is commonly limited to the intra- 
follicular regions, though rarely mycelial threads extend above 
this portion. 

It is at times difficult to differentiate these fungi, and person- 
ally I believe the diagnosis rests largely with the clinician. Cultural 
studies are recommended by some authors as giving a satisfactory 
method of distinguishing the 
different fungi known to play 
the part of the exciting cause 
of the ring- worm. It is not 
uncommon to find, in con- 
junction with ring-worm, 
small pustules, which are 
due to a secondary infection 
with pus-producing organ- 
isms. 

Tinea Circinata. — 
Patches of Tinea circinata 
occur over the body in more 
or less circular, solid, pale- 
red blotches covered with 
branny scales. Remove some 
of the scales and also extract 
a few hairs. Thinly smear the scales upon a slide, fix, stain, 
and examine for spores and mycelia (Fig. 218). 

Tropic Tinea. — Tropic Tinea circinata may occur upon any 
portion of the body, and when studied microscopically, this 
disease will be found to be produced by a fungus, as indicated by 
the occurrence of many mycelia. 

Tinea Barbae. — Tinea sycosis (barber's itch) will be found, 
as a rule, to involve only the bearded portions of the body. It 
usually presents a folliculitis, with pustules which are distinguished 
from the coccogenic form of sycosis only by microscopic study. 
According to Saboraud's researches, suppurating Tinea sycosis 
is due to the Trichophyton megalosporon ectothrix (Fig. 219, a), 
which Crocker regards as an animal parasite. The parasite sur- 
rounds the hair, as do the parasites in the other forms of tinea 




Fig. 218. — a. Tinea circinata (microsporon); b, 
trichophyton (megalosporon). 



5IO 



DISEASES OF THE SKIN. 




Fig. 219.-0, Tinea barbae ; b. Tinea cruris (after 
Crocker). 



(tonsurans). Remove the hair from the infected area, treat it 
for one hour with hquor potassae, and examine it under a one- 
sixth or a one-eighth objective for segmented chains of the parasite. 

Mycotic Dermatitis 
(Dhobie Itch). — Under 
this name it is customary 
to include a number of 
varieties of erythema known 
to tropic districts. Accord- 
ing to Mason, "dhobie itch " 
proper is induced by the 
Microsporon minutissi- 
mum; but recent observers 
have shown that many of 
the conditions regarded as 
dhobie itch result from 
other micro-organisms. P. 
Manson also believes that 
some forms of the disease 
are produced by the Micro- 
sporon furfur (Fig. 220, a) and by the trichophyton. Major 
Charles F. Mason* writes as follows: ''There are at least three 
distinct forms of skin disease occurring in the regions indicated 
which are commonly known 



as dhobie itch : two of them 
are mycotic — those due to 
the Microsporon minutissi- 
mum and to the tricho- 
phyton, and one is bac- 
terial — pemphigus contag- 
iosus." These parasites are 
detected after the manner 
given for the Tinea sycosis. 
Both scrapings and cul- 
tures from the mycotic areas 
are liable to show bacteria, 
and the degree of irritation 
excited by their develop- 
ment is a moot question. 
In mycotic dhobie itch 

the scrapings from the festooned rings will be found to contain 
the trichophyton, "sometimes, however, when there is much 
mfiammation, these elements cannot be found" (Mason). 

* "N. Y. Med. Jour.," Aug. i, 1903, p. 221. 




Fig. 220. — a, Tinea versicolor (Microsporon 
furfur) ; b, onychomycosis (Trichophyton endo- 
thrix of nails). 



TINEA VERSICOLOR. 



5" 



Onychomycosis. — Onychomycosis is a term applied to a 
condition in which either the Trichophyton endothrix or the 
Microsporon minutissimum is found to invade the nails (Fig. 
220, b). The detection of the parasite in the nails is accomphshed 
as already described. 

"Gayle.** — "Gayle" is a variety of puerperal sepsis which 
affects ewes during the lambing season, and which is known 
among sheep-breeders as a very fatal disease. Persons who skin 
animals dead of this disease are liable to infect their hands. The 
infection first produces a small pimple, which soon enlarges and 
fills with bloody serum. Klein * has obtained from these blebs 
and vesicles an organism which he found to be the exciting cause 
of the infection, to which 
he gave the name " Staphy- 
lococcus haemorrhagicus." 
The organism produces 
hemorrhagic edema when 
cultures are injected into 
animals. 

Tinea Versicolor. — 
Pityriasis versicolor is a 
parasitic disease which 
usually involves the skin 
of the trunk and chest, 
and is characterized by 
patches of a brown color. 
The detection of the Micro- 
sporon furfur is accom- 
plished in the manner 
described under Tinea 
tonsurans. This parasite 

is one of the most characteristic fungi of the skin; its conidia 
are arranged in closely crowded, conic aggregations surrounded 
by the mycelia (Fig. 221). These conidia are larger, as a 
rule, than are those of the other forms of ring- worm. The 
mycelia are short and often unbranched; they may show seg- 
mentation and nuclei at regular intervals. Budding is not 
uncommon. 

Detection. — A method suggested by Crocker is to place 
scrapings from the patch on a glass slide, wash with ether to 
remove the fat, and, when the mass is spread thinly, flood with 
liquor potassie and examine under a cover-glass with a one-eighth 
or a one-twelfth objective. 

* "Brit. Med. Jour.," Aug. 4, 1807, ]\ 385. 




Fig. 221. — Mycelia and spores of fungus re- 
covered from scrapings of the pigmented patches in 
pinta (after Montoja y Florez). 



512 



DISEASES OF THE SKIN. 



Erythrasma. — Erythrasma is a vegetable parasite disease 
which produces brownish patches upon the skin. 

Pinta. — Pinta is a tropic vegetable disease causing mycotic 
growths upon the skin. Place scrapings from one of the mycotic 
areas upon a sHde, treat with liquor potassas for one-half hour, 
and examine under a cover-glass with a rather high-power objective. 
Many dichotomous filaments, which are, as a rule, fine and 
cylindric, but at times granular and beaded, are seen. In places 
the mycelia form a dense net-work. This fungus is probably 
closely alhed to the aspergillus. 

Blastomycetic Dermatitis. — A number of cases of this 
disease have appeared in the United States, and it has also been 
observed in foreign countries. 

Detection. — Remove a bit of a tissue from the advancing 

margin of the disease, and 
macerate for twenty-five 
minutes in a solution of so- 
dium hydroxid (25 per cent.) 
in order to destroy the blood- 
ceUs and bacteria. Pus taken 
from the small abscesses 
should be treated in a hke 
manner. A precaution which 
I should strongly advise is to 
treat both pus and tissue with 
ether in order to remove all 
fats, since to the inexperienced 
eye oil-globules resemble 
yeast-cells very closely. After 
treatment with sodium-hy- 
droxid solution the yeast-cells 
are seen as highly refracting 
bodies, varying from 5 to 20 [i in diameter (Fig. 222). Cells 
in the stage of budding are commonly found. A one-sixth or a 
one-eighth objective will be found most serviceable in the study of 
this fungus. 

A closely aUied fungous disease was first described by Wer- 
nicke in 1890, and has been studied by Gilchrist, of Baltimore. 
Ophiils and Mofiitt, on the other hand, concluded that the disease 
is caused by a fungus which closely resembles that of blasto- 
mycosis. Five cases of generalized blastomycosis have been re- 
ported. The parasite has been found in pus and may appear 
in the sputum where the lungs are involved. 

Mycetoma. — Mycetoma is a fungus growth 




Fig. 222. — Blastomyces ; different forms of 
the fungus ; two budding cells ; small bodies are 
leukocytes. 



of the foot 



MYIASIS. 



513 



known, especially in tropic districts, as "Madura foot." V. 
Carter detected a fungus in the black variety of this disease 
("Chionyphe Carteri"). 

Detection. — Secure scrapings or a portion of the diseased 
tissue, macerate them in ether for twenty minutes, wash in sodium- 
hydroxid solution, and then smear upon a shde. Fix by heat, 
stain wath one of the ordinary anilin dyes, wash in water, and 
examine under a one-sixth or one-eighth objective. The fungus 
appears not unlike that of actinomycosis, and displays many 
small round bodies. Mycelia which are sometimes clubbed 
may be found. 

The mycetoma fungus grows extremely slowly in a hydrogen 
atmosphere, on a special medium composed of 100 parts of a 
2 per cent, infusion of hay 
or potato ; 9 parts of gela- 
tin; 4 parts of glycerin; 
and 4 parts of grape- 
sugar. Both black and 
white fungi are at times 
recovered. An exhaustive 
description of this disease 
is to be found in Hanson's 
"Tropical Diseases," 
third edition, page 680. 

Myiasis. — Myiasis is 
a disease produced by the 
screw-worm. The screw- 
worm (Fig. 223) is the 
larva of a dipterous insect, 
Chrysomyia mascellaria, 
common in certain por- 
tions of x\frica and in North and South America. The adult 
female (Fig. 223) deposits her eggs on the surface of a wound, 
in the external auditory meatus, and in the nasal fosStT, from 
which ova the larvae are developed. The larvae arc white, from 
one-half to three-quarters of an inch in length, and are formed 
of twelve segments. Each larva is circled with a spiral-like 
spine so arranged as to give the parasite a screw-like appearance 
(Fig. 223). 

Clinical Location. — These larva" are known to burrow 
through the tissues, destroying the mucous membrane, the muscles, 
and the cartilages. They may invade the serous sacs and the 
bones, producing extensive lesions. They have also been re- 
covered from the interior of the eye and the conjunctiva\ 
33 



^ 


A 






r 




/ '\ 





Fig. 223. — Screw-worm : A, Fly that deposits her 
ova on ati open wound ; A', larva American parasite 
(Blanchard). 



514 



DISEASES OF THE SKIN. 



George Gray * has reported five instances in which the larvae 
of the screw-worm w^ere found in human beings. He further 
stated that the parasite is common in domestic animals and that 
it is widely distributed throughout America. 

Vera Macaque. — Vera Macaque is the larva of an American 
insect (Dermatobia cyanicentris v. noxiahs, Fig. 224). The larva 
shows many circular bands from which extend fine spines. 

Impetigo Contagiosa. — During the past few years much dis- 
cussion has arisen as to the etiology of impetigo contagiosa. On 
account of its prevalence among students, it has acquired the names 
of "foot-ball impetigo" and "scrum-pox." These small lesions, 
whether vesicular or pustular, are due to inoculation with pus 
cocci, which are introduced into the superficial layers of the skin. 




Fig. 224. — Dermatobia noxialis : an American fly. Ova are deposited into skin of animals 
and in man ; B, Adult fl\- ; B', larva (Blanchard). 



Collection. — Collect either the pus or the serum directly from 
one of the lesions, smear it thinly upon a shde, fix by heat, and 
stain with carbolfuchsin, as for the tubercle bacillus, counter- 
staining with Gabbett's acid methylene-blue solution. The usual 
findings are streptococci, staphylococci, and diplococci. The 
streptococci are usually arranged in short chains of from four to 
six cocci each, although longer chains are at times observed. The 
clusters of staphylococci are almost equally common; but the 
diplococci are more rare. There seems to be a diversity of opinion 
as to the specific organism of this disease. It is stated that the 
impetigo contagiosa of Tilbury Fox is primarily vesicular and 
due to the streptococcus, w^hile others consider it due to a specific 
micrococcus. The Staphylococcus pyogenes aureus and the 

* "Brit. Med. Jour.," Mar. 28, 1903. 



ECZEMA. 515 

Staphylococcus pyogenes albus are common findings, wtiile the 
streptococcus of Fehleisen may occasionally be recovered from 
the vesicles. In the pustular variety and also in the vesicular 
form a mixed infection is not uncommon, and from my own 
observations both streptococci and staphylococci seemed to be 
capable of exciting the disease. 

Erysipelas. — It is possible to recover bacteria from the serum 
contained in the blebs of erysipelas and also from the blood 
exuding through minute punctures made in the infected areas. 
The exudate, pus, and blood, when smeared on a shde, fixed, and 
stained will, in the majority of instances, contain streptococci ; and 
Fehleisen has described a special streptococcus which he regards 
as the cause of this disease. I have isolated this streptococcus 
from a number of cases of erysipelas, and have succeeded in pro- 
ducing a similar condition in animals by inoculations. The 
Staphylococcus pyogenes albus, the Staphylococcus pyogenes 
aureus, and diplococci may also be found. Pfahler recovered only 
diplococci from a large number of cases of erysipelas which he 
studied at the Philadelphia Hospital. It was my privilege to 
examine many of the animals inoculated with this diplococcus, 
and the conditions excited by it were apparently identical with 
those caused by inoculation with the Streptococcus pyogenes and 
the Staphylococcus pyogenes. The above-mentioned bacteria may 
be cultivated from the skin overlying the erysipelatous areas. 
From a series of inoculations upon animals I am led to beheve 
it possible for erysipelas to be excited by any one or several of the 
pus-producing organisms. The tissue changes excited by the 
diplococcus, the Streptococcus pyogenes, and the staphylococcus 
were apparently identical. 

Eczema. — Probably one of the most important fields in which 
chnical laboratory studies have contributed to dermatologic diag- 
nosis is the study of parasitic eczema. An admirable paper upon 
this subject appeared from the pen of Professor Jadassohn, of 
Bera.* Unna has long claimed that certain forms of eczema are 
caused by a micrococcus, and many investigators have found 
staphylococci in the lesions. This germ is not only associated 
with the impetiginous variety of eczema, but also with simple 
forms. By cultural studies the Staphylococcus pyogenes aureus, 
the Staphylococcus pyogenes albus, and, in some instances, the 
streptococcus may be detected. 

While subject to numerous modifications, eczema appears like 
any ordinary wound infection; and since it is a disease of the 
derm, it is most likely to favor the development of the bacteria 

* "Wien. med. Presse," Aug. 5, 1900. 



5l6 DISEASES OF THE SKIN. 

known to inhabit the skin. Unna conducted cuUural studies of 
several cases, with the recovery of the following organisms: a 
staphylococcus which produced a white growth — the Staphylo- 
coccus pyogenes aureus; the Torula alba, and the Penicilhum 
glaucum. The cultural features of these organisms have been 
described in detail.* In view of the fact that many varieties of 
bacteria must of necessity be obtained from the cutaneous surface, 
it is difficult to show conclusively that Unna's coccus of eczema 
is the exciting cause of the disease; and while it or some other 
specific organism may cause the initial changes, infection with 
other organisms must certainly follow before the disease has made 
much progress. 

Conditions of Bacterial Origin. — The Staphylococcus pyo- 
genes aureus, albus, and citreus may be found either in pure 
culture or in conjunction wdth other bacteria in the following dis- 
eases, for which reason it has been deemed unwise to give the 
individual clinical appearances: Pemphigus contagiosa and pem- 
phigus neonatorum; dermatitis papularis capilhtii, and possibly 
other forms of pustular folliculitis; Quinquaud's folliculitis decal- 
vans; impetigo of Bockhart, and other forms of impetigo sycosis 
(coccogenic and lupoid); boils, carbuncles, and abscesses; ery- 
sipelas, in which streptococci, staphylococci, diplococci, Pfahler's 
diplococcus, and the colon bacillus may exist; superficial whitlows; 
granuloma pyogenicum, and acne. 

The Streptococcus pyogenes and the Streptococcus pyogenes 
of Fehleisen are found primarily in the following conditions : super- 
ficial whitlows, impetigo contagiosa, ecthyma, erysipelas, and 
erysipeloid processes. It is to be borne in mind that in any of 
these cutaneous lesions a mixed infection is common, and that 
bacilli are not infrequently detected in symbiosis with the patho- 
genic cocci. Furthermore, the lepra bacillus, the tubercle bacillus, 
and the bacteria of glanders, which have been considered else- 
where in this volume, may also be recovered from the individual 
lesions of these diseases. 

Oriental Sore — J. H. Wright f has found that a peculiar para- 
:site infests the tissues in tropical ulcers. There is yet some ques- 
tion as to the nature of these bodies. Christophers suggests the 
■possibility of this being the Leishman-Donovan parasite (see page 
525.) 

* "N. Y. Med. Jour.," Sept. 29, 1900, p. 547. 
t "Jour. Med. Research," 1904, p. 472. 



CHAPTER XIII. 



MILK. 



The mammary secretion may be obtained from the breasts 
of the human female during the period of gestation and of lactation. 
It usually makes its appearance in the mammary gland some time 
after the third month of pregnancy, after which it gradually in- 
creases in quantity, reaching its maximum about three days after 
labor. 

COLOSTRUM. 

Colostrum is a watery, slightly turbid fluid, which may 
be expressed from the breasts during the period of gestation, and, 

in rare instances, is to be ^ — ^_^^^^ 

obtained independently of /^oS '*^%° o^^^^ 

gestation and even from Z^" A^, Q o ^\ 

the male breast. A vari- / ",, O c o^ |iO \ 

able quantity of this fluid / H-i^-^O. ^^O^ ' ^ t» Oo\ 

is always secreted during L 0)r^ 6„ ^^ ^ \ °\ 

the latter half of gestation /©"o '^C.J o ^ "* o ^ °CJ> q ^ \ 

and immediately after par- \° '''''"* ''O^/ * ?^^,C)^- 0&^^ 

turition, when it may be Q^o^o CP O ^^ °r> ^^""^o*^ 

highly tenacious, resemb- \ ^ ^^ '^ lu^. O^ V® "^Q ''°7 

ling mucilage, and may W^ ^""^^^^0 "^"^/d ^ QO" V 

vary in color from a pale- Vg O^l, " ^O ^ ^0^~^^-O / 

gray to an orange-yellow. \^^C)0 " ^4K^^0'>; .-^y 

Distinctive Features. Xi"o ^ ^^0 V^^ X 

—The features that dis- ^-2!^£0«J^>-^ 
tinguish colostrum from 

milk are the color densitV Fig. 225.— Colostrum from primipara. Fat-drop- 

mUK are me LOIOI, UCllbliy, lets, two colostrum corpuscles, and one epithelial cell 
tenacity, the high percent- (obj. Queen one-twelfth oil-immersion). 

age of sugar and salts, 

and the property of the former of coagulating when heated to the 
boiling-point. According to Dunghson, the following chemic 
differences are known to exist between colostrum and normal milk: 

Colostrum. Normal Milk. 

Water 828 887.6 

Fat 50 253 

Casein 4° 34-3 

Milk-sugar 7° 48.2 

Ash 3 2.3 

517 



Si8 



MILK, 



According to repeated analyses, casein does not appear in 
colostrum in appreciable amounts until after parturition. 

Microscopy. — When examined microscopically, colostrum 
will be found to be composed of fat-droplets, leukocytes, epithelial 
cells, and the so-called colostrum corpuscles. The fat-droplets are the 
principal constituent and are usually quite small. The colostrum 
corpuscles are highly refractive, granular bodies, which vary 
greatly in size and are composed of many minute fatty granules 
(Fig. 225). Fixed specimens of colostrum when stained with 
Sudan III or with osmic acid show the presence of fats. 



HUMAN MILK. 



The quantity of milk secreted in twenty-four hours varies 
between 500 and 1500 c.c. It is usually of a bluish color, alkaline 
reaction, and displays a specific gravity between 1.026 and 1.033 
(the majority of specimens are near 1.030). ]\Iilk when subjected 
to a microscopic examination will be found to be a fairly homo- 
geneous emulsion of fat, containing but few, if any, cellular ele- 
ments. Dunglison gives Simon credit for the following table of 
comparison : * 





Human ] 
Variations. 


Average. 


Cow's ^ 
\'ariations. 


IlLE. 

Average, 


Goat. 


Sheep. 


Ass. 


Mare. 


Water .... 
Casein and albumin 
Fat (butter) . . 
Lactose .... 
Inorganic salts . 


90.4 to 85. 7 
i.§ •• 3-1 
3-0 " 3-8 
4-5 " 7-0 
0.3 " 0.4 


88.05 
2-45 
3-4 
5-75 
0-35 


90.2 to S3.7 
3-3 " 5-5 
2.8 " 4-5 
3-0 " 5-5 
0.7 0.8 


86.95 
4.4 
3-65 
4-25 
0.75 


86.0 
3.8 
5-2 
4-3 
0.7 


833 

It 

11 


90.6 

2-7 
I.O 

5-3 

0.4 


90.6 
2.2 
I.I 
5-8 
0.3 



SKIililED COXDEXSED 



Milk. 



Water 89.6 

Casein and albumin . I 4.2 

Fat (butter) . . . . j i.o 

Lactose 4-4 

Inorg-anic salts ... 1 0.8 



Milk. 




Butter. 



15.0 
2.2 



0-3 



iUTTERMILK. CURD. , WhEY. 



91.0 
3-7 

0.8 
3-8 



59-4 
27-7 
66.4 
5-0 

1-5 



93-8 
0.8 
0.3 
4-5 
0.6 



Certain albumins, such as casein, lactoglobulin, and lacto- 
albumin, are found in milk. There are certain differences between 
the casein of human milk and the casein of cow's milk: first, it 
will be noticed that the casein coagula formed in human milk are 

* Dunglison, twenty-third edition, p. 712. 



HUMAN MILK. 519 

smaller and less dense than are those seen to form in cow's milk. 
Human casein is precipitated by acids and salts, but it is less 
readily precipitated than is the casein from cow's milk. Again, 
human casein may not coagulate after the addition of a rennet 
ferment. Furthermore, human casein is precipitated by gastric 
juice, an excess of which causes dissolution. Hammarsten, in 
addition to the above points of difference, states that the two 
forms are not identical; but for practical clinical purposes their 
differences concern us but little. 

Bacteria. — According to Welch, normal human milk is likely 
to become contaminated with the Staphylococcus epidermidis 
albus while passing from the acini of the gland through the lactifer- 
ous ducts and the nipple. It is to be borne in mind that this 
organism is constantly present in the skin, but that it is by no 
means the only bacterium common to cutaneous surfaces or known 
to invade the glandular portions of the skin; it appears, however, 
to be the only organism common to human milk. At times the 
Staphylococcus pyogenes aureus may be found in human milk. 

Pathologic Milks. — Milk obtained from nursing women 
during the course of febrile attacks and during the existence of 
diseases associated with emaciation is Hkely to be deficient in fat 
and in lactose. During the course of jaundice biliary pigments of 
doubtful authenticity are said to have been recovered. In cases 
of malignant tumor of the mammary gland and after traumatism 
bloody milk has been observed. Microscopically, the milk ob- 
tained from a diseased breast is likely to show a large number of 
leukocytes, a finding most marked in connection with mammary 
abscess. A number of pathologic micro-organisms may invade the 
mammary secretion during disease — e. g., during puerperal fever 
streptococci and staphylococci may occasionally be found. The 
pneumococcus has been recovered from the milk of nursing women 
suffering from lobar pneumonia, and in one instance, a case studied 
at the Philadelphia Hospital through the courtesy of Dr. George I. 
McKelway, I recovered a pure culture of the pneumococcus from 
the milk. In a second case studied the milk obtained from a 
woman suffering from typhoid fever gave a pure culture of a 
bacillus which agglutinated with the patient's blood (dilution 1-40) ; 
further tests for the Bacillus typhosus were not conducted. The 
milk of women suffering from typhoid fever will be found to 
agglutinate typhoid bacilli (see Serum- diagnosis, page 116). 

Tubercle Bacilli. — Tubercle bacilli may appear in the milk 
of women suffering from tuberculosis. Roger and Garier * 
report the case of a young woman who was suffering from both 

* "Sem. Med.," Feb. 23, iqoo, 2ome Annec, No. 9. 



520 



MILK. 



pulmonary and laryngeal tuberculosis and who died seventeen 
days after delivery. The milk was found to contain tubercle 
bacilli, and the child which nourished upon the breast-milk for a 
few days eventually died of tuberculosis. Subcutaneous inocula- 
tion of a guinea-pig was also fatal, the animal developing tubercu- 
losis which terminated fatally thirty-three days after inocula- 
tion. 

The milk of cows may be colored blue or green by the Bacillus 
pyocyaneus; and it appears reasonable that this organism or 
any other chromogenic bacterium when present in human milk 
would color that fluid. 

It should always be borne in mind that the Micrococcus 
prodigiosus and the Bacillus prodigiosus produce a decided red 
growth, and that when the former of these organisms develops in 
milk, that fluid is liable to present a reddish color after it has been 
allowed to stand for a short time at room-temperature. 

Detection of Bacteria. — Fill one tube of a centrifuge nearly 
to its top with the suspected milk, and fill the 
other tube with a dilution of one part of the 
suspected milk and three parts of sterile water; 
centrifugalize for five minutes; then pipet the 
sediment from each tube and place it upon 
separate slides, smear thinly, and fix by heat. 
Stain such smears with a 2 per cent, aqueous 
solution of methylene-blue and with carbolfuchsin 
and Gabbett's solution as directed for determin- 
ing the presence of tubercle bacillus (see page 
438). Both cocci and bacilli are usually found 
in this manner. 



Fig:. 226.— Que 
venne's lactoden 
simeter. 



SPECIFIC GRAVITY. 

The specific gravity of milk is determined by 
the lactodensimeter of Quevenne. The instrument 
is standardized at a temperature of 60° F. (Fig. 
226), so that a correction of the reading obtained 
at any higher temperature is necessary. The 
table accompanying each instrument should be 
consulted for this correction, and will indicate the true specific 
gravity when the temperature is between 46° and 75° F. This 
rather tedious process is readily avoided by heating the specimen 
of milk to a temperature of 60° F., when the Quevenne instrument 
will register accurately. 

Author's Method. — The method I employ for this purpose 



ESTIMATION OF FAT. 



521 




Fig. 227.— Plane cylin- 
dric glass. 



is to place a thermometer in a glass jar containing warm water 
and to contmue adding warm water to this jar until the tempera- 
ture of the water reaches 60° F. The milk 
is then placed in a small glass cylinder (Fig. 
227), which, with its contained milk, is stood 
in the warm water. The thermometer is 
then removed from the water, the mercury 
shaken down, and the temperature of the 
milk taken. When the milk reaches 60° F., 
the thermometer is removed and the lacto- 
densimeter introduced. The specific gravity 
is read from the graduation on the instru- 
ment. This method has always appealed to 
me as most practical, and, since it necessi- 
tates but little extra work and no task of 
memory or reference to tables, I think it 
deserves recommendation to the profession. 
It is difficult to believe that the person de- 
signing the lactodensimeter had any other 
idea in mind, since the instrument was certainly designed 

for the purpose of simplifying laboratory 

methods. 

ESTIMATION OF FAT. «. 

The fat present in a given specimen of 
milk is most conveniently estimated by the 
lactoscope designed by Feser (Fig. 229). Fill 
the pipet with milk to the mark (M) and trans- 
fer this quantity of milk into the cylinder (C). 
Then attach a dropper to the tube at (P) 
and rinse the pipet thoroughly by forcing 
water through it, adding all the wash-water 
to the milk in the cyhnder. The milk and 
wash-w^ater are then shaken together, and 
more water is added slowly from a buret 
until the black hnes on the glass plug (A) at 
the bottom of the cylinder become discernible. 
The cylinder is then held in a good light in 
order to view the graduated scales upon its 
right and left margins. The point on the right 
scale to which the mixture extends indi- 
cates the percentage amount of fat present; 

while the point on the left scale represents the amount of 

water in cubic centimeters that has been added. 



Fig. 228.— Milk tube. 
These tubes are used in 
placeof theregularsedi- 
mentation tubes, and are 
graduated to give per- 
centage of fats in milk 
according to the Leff- 
man-Beam or Babcock 
method. Very useful for 
human as well as for 
cow's milk analysis. 



522 



MILK. 



All-important in the use of this instrument is that both the 
cylinder and the pipet be thoroughly cleansed 
c. after use. 



^ 



10- 



-M 



Fig. 229. — Feser's lac- 
toscope. 



ESTIMATION OF PROTEIDS. 

Woodward^s Method. — Two milk burets 
are necessary for this purpose. In each 
of these burets 5 c.c. of the milk to be anal- 
yzed are placed and the burets kept at a 
temperature of from 37° to 40° C. (98.6° to 104° 
F.) for from eighteen to twenty-four hours. At 
the end of this time the milk will be found to 
have separated into two layers: the superior 
layer is composed of a viscid, yellowish fat, 
w^hile the inferior layer is composed of a more 
or less markedly opalescent fluid. A granular 
precipitate may also be seen at the bottom of 
the buret and clinging to the sides of the instru- 
ment. Now place both burets in a cool place 
and withdraw the milk- serum (inferior layer) 
from each buret into a separate tube gradu- 
ated to 15 c.c, and add Esbach's reagent 
(picric acid, 10 grams; citric acid, 20 grams; 
water, 1000 c.c.) to the 15-c.c. mark. Stir 
the mixture in each tube thoroughly by means 



of a glass rod, and centrifugalize to a constant reading. 



ADDENDA. 



BLOOD. 

TORKRITIZATION. 

A clinical instrument introduced by H. E. Wetherill in 1894, 
and has been in use in my laboratory during the past few mionths. 
This unique and practical apparatus consists of a metal armature 
which is provided with two receptacles for the tubes. This arma- 
ture is revolved upon a twisted cord (Fig. 230), and speed depends 




Fig. 230.— Wethei'ill's torkrit. 

directly upon the length of the cord and the number of pulls per 
second. Wetherill claims that a speed of 25,000 revolutions a 
minute is readily obtained, and that the exact rate of speed is of 
little consequence since it is already too high to permit of error 
(see Torjugation, p. 528). 



BIFFS HEMOGELOMETER. 



A test-tube, 25 centimeters long and 4 centimeters wide, is 
filled to one-half its depth with water. Provide this tube with 
a cork stopper containing two openings. Through one opening 
a thermometer passes and through the other a glass rod, at one 



523 



524 



ADDENDA. 



extremity of which is a platinum wire coiled so as to form five 
loops, three millimeters in diameter, the one above the other. 

Heat the water to 68° to 70° Fahr. Fill each loop by touch- 
ing it to the summit of a drop of blood, and in from three to five 
minutes later place the glass rod into the cork and submerge the 
lower drop of blood, when, should it be diffused into the water, 
continue to immerse the successive loops at intervals until one 
of them is not diffused. Xote the coagulation time. The time 
required for normal blood is from seven to ten minutes. 



WETHERILL'S ANTE-MORTEM BLOOD COLORS. 

This color-scale is a most ingenious one, and is doubtless an 
accurate test for the percentage of oxyhemoglobin (Fig. 231). It 
approximates more closely the color of the blood than any other 




Fig. 251.— Wetherill's hemoglobin scale. 



printed scale I have been privileged to examine. The technic 
for its employment is given in each booklet. 

Wetherill's booklet also contains color-scales for postmortem 
blood, urine, moisture (degree of perspiration), and for the feces. 



POLYGLOBULLA.. 

This is a condition showing, in addition to polyc}1:hemia, 
cyanosis and enlargement of the spleen (usually tubercular). 
Vaquez was the one first to give an accurate clinical picture of 
this chronic condition, and at present reports of 30 cases have 
appeared in the literature.* 

* M. Ascoli, "Riformi Medica," Dec. 21, 1904. 



BLOOD. 



525 



The red blood-cells may reach 9,000,000 to 12,000,000 per 
c.mm. When leukocytosis exists it concerns the polynuclear cells 
chiefly. At times mast cells are common and eosinophilia may be 
present. As a rule, there is an excess of hemoglobin, but in a 
few instances the hemoglobin was below the normal. The specific 
gravity is increased and has reached 1.080. 

PICKER'S TYPHOID REACTION. 

This reaction depends upon the clumping of dead typhoid 
bacilli. Three small tubes are partially filled with a fixed quantity 
of bouillon culture. 

Method. — Examine each tube to determine that the serum 
it contains is slightly cloudy, due to bacilli in suspension. To 
the first tube add a certain quantity of blood-serum (dilution 1-5); 
to the second add the same quantity of dilute serum (i-io). 
The third tube is used as a control. The reaction consists in a 
clearing of the liquid and the formation of a precipitate in tubes 
one and two, while tube three remains unchanged. 

LEISHMAN-DONOVAN BODY. 

A questionable parasite first well described by Surgeon Leish- 
man and later detected in persons suffering with "dum-dum" 
fever, kala-azar, Delhi sore, and tropical anemia by Donovan, 
Jas. H. Wright and others. 

The Parasite. — As generally seen it is of an elliptic shape, 
varying from ij to 4 microns in length by from i J to 2 microns in 



i;^ , .-f^. 9 f^ (^ 



Fig. 232. — Leishman-Donovan bodies. 




breadth. The smaller bodies may be more fusiform in contour; 
the larger ones more nearly circular. Christophers compares 
its shape to a closed cockleshell. A characteristic feature is its 
double nucleus. All except the smallest forms present a rather 
large oval nucleus near the periphery and anotlier small rod- 



526 ADDENDA. 

like nucleus on the opposite side (Fig. 232). In this respect 
the parasite resembles the degenerated forms of the trypano- 
some. 

The parasite stains by the various modifications of Romanow- 
ski's method, and then a well-formed capsular wall is apparent. 
The larger parasites often display vacuoles and their body sub- 
stance is stained a bluish-pink color. Christophers has observed 
the larger nuclei dividing, but the rod-like body remains un- 
changed. Large spheric bodies containing what appears to be 
dividing parasites are also seen. Bodies of this type are seen 
to contain from 3 to 18 small parasites. 

Leonard Rogers* has cultivated the Leishman-Donovan 
parasite on artificial medium at a temperature of 22° C. Other 
observers have found the parasite to develop luxuriantly at a tem- 
perature of 18° C. Rogers states that he has developed a trypano- 
some from these bodies of Leishman-Donovan; and Chatterjee 
has confirmed the work of Rogers. t This trypanosome resembles 
that originally described by Keysselitz (see trypanosome, p. 151). 
Stimulated by Schaudinn's observation that the intracorpuscular 
pigmented parasite becomes a trypanosome, we should consider 
the many possibilities of this Leishman-Donovan parasite play- 
ing some part in the role of atypical malaria. 

Detection of the Parasite. — I have been able to find but 
two references to the parasite's detection in the peripheral cir- 
culating blood. Nearly all authorities agree that the parasites 
are readily detected in the fresh blood obtained by puncture of 
the spleen. Splenic puncture is said to be extremely common 
among general practitioners of the tropics, but in subtropical dis- 
tricts such procedure should be conducted by the surgeon. 

Smear the fresh blood thinly upon a slide, add a cover-glass, 
and study under a y 3- oil-immersion objective, as with the malarial 
parasite (see Malaria, p. 157). 



URINE, 

RAVOLD^SJ COMBINED HEAT AND CONTACT TEST FOR 
ALBUMIN. 

Reagent. — Dissolve 2 gm. of corrosive sublimate; 4 gm. of 
succinic acid, and 4 gm. of common salt in 50 c.c. of water. After 
standing for a few hours add 50 c.c. of a saturated solution of 

* "Brit. Med. Journ.," Sept. 17, 1904, p. 648. 

t "Lancet," Jan. 7, 1905. 

X "Jour. Mo. State Med. Assoc'n," April, 1905. 



URINE. 527 

magnesium sulphate; shake to effect a perfect mixture and the 
reagent is ready for use. Keep in a glass-stoppered bottle. 

1. Unless clear the urine should be filtered, and to 5 c.c. of 
the filtrate add i c.c. of acetic acid. 

2. Fill a test-tube to one or two inches in depth with the 
reagent. 

3. Add, by means of a pipette, J to i c.c. of acidified urine 
(permitting the urine to float upon the reagent). A ring of albu- 
min may appear at the zone of contact of the urine with the 
reagent. 

4. Heat gradually to boiling. The ring thus produced tends 
to remain. 

Ravold has found this test of value for the detection of minute 
amounts of albumin. Ravold 's reagent may be heated in a test- 
tube and applied after the author's contact method, p. 207. 

CLINICAL SIGNIFICANCE OF ALBUMIN. 

For convenience of study albuminuria may be considered 
under the following subheads : 

I. Renal albuminuria, — a condition where the albuminous 
body escapes with the urine into the uriniferous tubules, or, 
less often, enters the urinary tract at the kidney's pelvis. In 
either case the condition inducing such escape of albumin is 
inflammatory. During the early stage of acute nephritis the 
amount of albumin is very large, and may equal from one-tenth 
to one-half the quantity of the urine by bulk. A large amount 
of albumin is also present during the entire course of chronic 
parenchymatous nephritis; the amount of albumin ranging 
inversely to the quantity of urine. Toxic albuminuria indicates 
a condition where albuminuria follows large doses of renal irri- 
tants, or where it develops during the course of acute infections 
(diphtheria, scarlet fever, typhoid fever, etc.). 

Throughout the course of chronic interstitial nephritis, and 
also where there exists amyloid disease of the kidneys, the amount 
of albumin in a given quantity of urine is relatively small; but 
when one considers the quantity of urine voided during the 
twenty-four hours and the percentage amount of albumin correla- 
tively, it will be seen that considerable albumin is lost daily. 
During an acute exacerbation of chronic nephritis the quantity 
of urine is also small and the amount of albumin relatively 
large. 

Traumatism in the region of the kidneys, pressure, and mas- 
sage of the loins and abdomen may cause albuminuria. 



528 



ADDENDA. 



2. Albumin may escape into the urine as a result of blood 
dyscrasia, e. g., leukemia and the severer secondary anemias, and 
particularly after chronic mineral poisoning. 

3. Parasitic albuminuria is seen during infection with the 
filaria, schistosoma, hematobium, and other parasites (see pp. 
292 to 300). 

4. Inflammatory processes of the bladder, prostate, and 
urethra are frequent sources of albumin. It may at times depend 
upon the escape of seminal fluid with the urine and is usually 
present in the first urine voided by the male after intercourse. 
In the female it is very common to find albuminous bodies present 
in the urine voided by the patient; while the urine obtained by 
catheter is albumin-free. 

6. Intermittent, cyclic, transitory and digestive albuminuria 
concerns us only in that persons suffering from any one of these 
forms of albuminuria will in the majority of instances develop 
true albuminuria later. Here the albumin is of renal origin and 
suggests an unbalancing of the functions of metabolism and 
renal secretion. 

TORFUGATION. 

Wetherill's centrifugal method depends upon the revolution 
of a tube-containing-bar upon a twisted cord (Fig. 233). The 
motions are to and fro, and a speed of 5000 revolutions a minute 




1 

may be obtained. This method provides a most practical means 
for the recovery of urinary sediments; and for the rapid estima- 
tion of albumin by the Esbach method ; and for centrifugal anal- 



URINE. 



529 



ysis in general (except milk). The torfuge has found a useful 
field in clinical laboratory methods (see torkrit, p. 523). 



QUANTITATIVE ESTIMATION OF PURIN IN THE URINE. 

The purin bodies excreted with the urine include combinations 
containing the nucleus CjN^ (see Uric Acid, page 196). For con- 
venience of study the purin bodies of the urine are classified into 
exogenous and endogenous purins, the former being derived from 
the foods, and therefore bearing a direct relation to the amount of 
purins taken as food. The endogenous purins are thought to 
result from the nucleins of the body, and therefore their estimation 
serves as an indication of the degree of dis- 
integration resulting from metabolism. 

Method of Determination. — C a merer 
offers the following method for the determina- 
tion of the amount of purin bodies in the urine : 

Reagents : 

1. Ludwig's magnesia mixture * loo c.c. 

Ammonia (20 per cent.) 100 c.c. 

Talcum 10 gm. 

2. Silver nitrate i gm. 

Ammonia (pure) 100 c.c. 

Talcum 5 gm. 

Distilled water 100 c.c. 

Instrument. — The purinometer (Fig. 230) 
consists of a graduated cylinder which is 
divided equally into halves, these halves being 
separated by a perforated cork. 

1. Place 90 c.c. of the mixed twenty- four 
hours' urine, free from albumin, and 20 c.c. of 
reagent into the superior half of the purinom- 
eter. 

The object of this procedure is to throw 
out of solution the urinary phosphates which collect at the bottom 
of the tube, upon the upper surface of the cork. 

2. After ten minutes turn the cork and permit the sedimented 
phosphates to pass into the lower half of the purinometer, and 
then return the cork to its former position. 

3. Add to the remaining urine in the superior half of the 
purinometer reagent 2, filling to the graduation 100. A precipitate 
results which is composed of silver chlorid and silver purin; but 

* Crystalline magnesium chlorid, loo gm.; Water, looo c.c; .\ninionia, 
sufficient to give the solution a strong odor; and Ammonium chlorid, enough to 
dissolve all precipitate that may result. 
34 




Fig. 234. — Purinometer. 



530 



ADDENDA. 




the former., silver chlorid, is dissolved by the excess of ammonia 
present. 

4. The precipitation of the purin bodies present 
in the urine is hastened by agitating the hquid after 
the addition of reagent 2. Whenever the yellow 
silver urine precipitate is seen to contain v^hite floc- 
culi, add a few drops of ammonia to the mixture. 

5. Place the purinometer in a dark room for 
from one to twenty-four hours, after which it 
should be brought to the hght and the precipi- 
tated silver purin read from the graduation upon 
the instrument. 

6. Multiply the number of centimeters of the 
precipitate by 1.5 (percentage), and the empyric 
value, approximately o.ooio (which is determined 
for each apparatus), gives the percentage of nitro- 
gen. The figure thus obtained, when multiplied 
by the daily amount of urine expressed in cubic 
centimeters, and this product divided by 100, 
will give the total amount of purin nitrogen ex- 
creted during the twenty-four hours. With each 
purinometer is furnished a special table by the 
aid of which the percentage of purin nitrogen is 
readily estimated. It has been found that the 
most satisfactory results are to be obtained with 
urines of a specific gravity between 1.015 and 
1.025; and it has been further found that the 
ingestion of both tea and coffee interferes with the 
estimation of purin nitrogen; and that a diet 
composed of eggs, milk, rice, potatoes, bread, 
butter, and cheese is best adapted for the deter- 
mination of the endogenous purin excreted. The 
exogenous purin may be determined while the 
patient is taking indefinite quantities of meat. 



0.176 

0.17S 

.0,]81 

0,184 

0,187 

0.190 

0,193 

019S 

0.199 

0.202 

0.205 

0.209 

0.211 

0,215 

0.213 

0,221 

0.225 

0.223 

.0.231 

.0.235 

.0.238 

.0.242 

0.24fi 

0.249 

,0.254 

0.26 

.0,28 

.0.8 

0.33 

0,35 

0,88 

0,41 

0,44 

0.47 

0.5 

»-0.55 

9 -0,6 

0.653 

0.71 

0.76 



Fig. 235.— Ruhe- 
mann's uricome- 
ter. 



QUANTITATIVE ESTIMATION OF URIC ACID- 

Ruhemann's method for estimating the urinary 
uric acid is dependent upon the union of uric 
acid with iodin. The instrument employed is 
termed a uricometer (Fig. 231), and consists of a 
graduated glass tube 25 centimeters in length. 



URINE. 531 

Reagents. — i. Sulphid of carbon. 2. lodin solution. 

Potassium iodid 1.5 parts 

lodin 1.5 " 

Alcohol (absolute) 15 " 

Water 185 

1. Fill the uricometer to mark S with reagent i. 

2. Add 2 ex. of reagent 2, which fills the uricometer to mark I. 

3. Add slowly to the mixture acid urine free from albumin 
and from sugar, shaking well after each addition. The urine is 
added cautiously until the brown color gives way to that of white. 

4. Read the percentage of uric acid pro mille from the right- 
hand column of figures graduated upon the uricometer; and from 
the left-hand column read the number of cubic centimeters of 
urine employed. 

Caution. — Where the amount of uric acid present is too small 
to register, it is advisable to employ one-half or one-fourth the 
quantity of iodin solution. 

GLYCERIN. 

Cammidge's Reaction.— -The so-called ''Cammidge's re- 
action" depends upon the recognition of glycerin in the urine, 
and the test is practically that for glycerose. The local fat nec- 
roses probably result from a selective action of the pancreatic 
secretion. The tissue fat is converted into the fatty acids which 
readily combine with lime; while the other constituent of the fat 
molecule, glycerin, is thus set free and enters the circulation, ap- 
pearing in the urine as glycerin, but is converted into glycerose 
by boiling with a mineral acid. Two tests, ''A" and ^'B," are 
described in detail for glycerose,* and both are modifications of 
the phenylhydrazin test for glucose p. 229. 

Reaction "yl." — i. Place 10 c.c. of filtered (sugar-free) urine 
into a flask. 

2. Add I c.c. of strong hydrochloric acid. 

3. Place a funnel in the neck of the flask to act as a condenser, 
and boil gently on a sand-bath for ten minutes. 

4. Add 5 c.c. of filtered urine, and 5 c.c. of distilled water; 
set the mixture in running water and allow to cool. 

5. Neutralize the excess of acid with 4 gm. of lead carbonate; 
add slowly, and allow to stand for five minutes. 

6. Filter through a moist filter-paper, and wash the flask upon 
the filter with 5 c.c. of distilled water. 

*" Lancet," Mar. ig, 1904. 



532 ADDENDA. 

7. To this filtrate add 2 gm. of powdered sodium acetate 
and 0.75 gm. of phenylhydrazin hydrochlorate ; boil for four 
minutes on a sand-bath. 

8. Cool, pour into test-tubes, or, better still, into the tubes of 
the centrifuge and centrifugalize. 

9. Transfer this sediment, by means of a pipet, to a slide, when 
study under a J objective. In the presence of disease of the pan- 
creas this sediment is found composed for the most part of fine 
needle-like crystals which may appear in dense aggregations or 
in sheaves. 

Fallacies. — This reaction is occasionally obtained with the urine 
of carcinoma, pneumonia, etc., where there is active tissue change 
taking place. 

Reaction "5." — This differentiating test depends upon the 
fact that the crystals — end reaction — seen in reaction "A" do 
not occur in pancreatic inflammations when the urine is first 
treated with perchlorid of mercury, while such preliminary treat- 
ment exerts no influence upon the reaction in cancer of the pan- 
creas, pneumonia, etc. 

1. Thoroughly mix 20 c.c. of filtered, sugar-free urine with 
10 c.c. of a saturated solution of perchlorid of mercury, and allow 
to stand for ten minutes. 

2. Filter and to 10 c.c. of this filtrate add i c.c. of strong 
hydrochloric acid. 

3. Boil for ten minutes in a sand-bath; dilute with 5 c.c. of 
the filtrate from step i and 10 c.c. of distilled water; cool in run- 
ning water and continue as in reaction "A," step 5. 

Clinical Significance. — {a) Should no crystals be found by 
either the "A" or the "B" method, the pancreas is healthy. 

{h) Should crystals be obtained by the "A" and not by the 
"B" method, active inflammation of the pancreas exists — an 
indication for surgical intervention. 

(c) The solubility of these crystals is studied by permitting 
acids to flow underneath the cover-glass while observing the crystals 
under the microscope. Crystals "A" dissolve in 33 per cent, 
sulphuric acid in one-half to one minute, where acute pancreatic 
inflammation exists. In chronic inflammation they require two 
minutes to disappear. Crystals obtained by both "A" and "B" 
methods are suggestive of pancreatic cancer. In cancer the 
crystals require five minutes to dissolve. 



GASTRIC CONTENTS. 533 

GASTRIC CONTENTS. 

CIPOLLINO^S TEST.* 

Reagents: (i) Anilin water; (2) a titrated solution of sodium 
hypochlorite; (3) a solution of hydrochloric acid 5 parts to 1000, 
for control tests. 

1. Place 2 c.c. of filtered gastric contents into a test-tube. 

2. Add one-half c.c. of anilin water and shake the mixture 
gently. 

3. Add drop by drop 4 or 5 drops of the sodium hypochlorite 
solution, shaking gently after each addition; and should the 
hydrochloric acid present not equal the normal, a yellow color 
results. Should the mixture become violet, repeat the test, using 
2 parts of gastric fluid with i part of distilled water; and a violet 
color now shows that there is more than 2 parts per 1000 of HCl 
present — the lower normal quantity. A faint violet color resulting 
after the employment of gastric fluid and distilled water in equal 
parts denotes that there is three parts of HCl per 1000 — the 
extreme limit for normal gastric fluid. A dark violet color is in- 
dicative of an excess of HCl; and should a faint violet color per- 
sist, the HCl is above normal. 

PURIN BODIES IN THE FECES.f 

According to Schittenhelm, the amount of purin nitrogen in 
the feces is in direct proportion with the amount of solid substance. 
This amount is directly influenced by diet; e. g., sl diet with much 
residue or one rich in nucleins (thymus gland) causes an increase. 
In diarrhea some of the food purins pass into the feces; and in 
disease of the pancreas due to incomplete digestion of nuclein 
the amount of purin in the feces is greatly increased. 

The purin bodies are decreased in the feces of alcoholism 
and in constipation. The intestinal wall contains purin basest 
viz., adenin, guanin, xanthin, and hypoxanthin; and it has been 
suggested that a portion of the purins in feces is derived from this 
source. Meconium contains uric acid but not purins (see Purins 
in Urine, page 529). 

MOISTURE OF THE BREATH. 

This is accurately determined by the aid of Wethcriirs hygro- 
scope; or by the color scale, page 524. 

* " Riforma Medica," Dec. 7, igo4. • 

t"Deut. Arch. f. klin. Med.," Bd. Ixxxi, p. 423. 



534 ADDENDA. 

Hold the open surface of the instrument or the sHp of litmus 
paper directly in front of the opened lips and direct the patient 
to exhale through his mouth. 

Clinical Significance. — The moisture of the normal breath 
approximates 85. The degree of moisture is increased in con- 
ditions where the skin and kidneys are inactive, and Wetherill 
found it to reach 95 in uremia. 



CLINICAL SIGNIFICANCE OF BUCCAL SECRETION IN DISEASE. 

The reaction of the saliva is acid in diabetes, neoplasm of 
the stomach, in leukemia, pernicious anemia, and occasionally 
in chlorosis. In uremia it may contain urea. Fleckseder* de- 
tected sugar in the saliva of 2 of 13 cases of diabetes studied. 

Oligosialia (diminished saliva) is to be seen in diabetes mel- 
litus and insipidus, severe diarrhea, profuse sweating, vomiting, 
dropsy, cachexia, gastric carcinoma, malignancy, the anemias, 
hepatic cirrhosis, in high fevers, and rarely after ptyalism. At 
such times the saliva is cloudy, tenacious, and emits a sweetish 
odor. 

Ptyalism is characterized by a clear, thin, alkaline secretion, 
which is decreased in rhodan. Ptyalism is met with in stomatitis, 
pregnancy, painful gastric maladies, gastric ulcer, and nausea. 
An intermittent increased flow of saliva is observed in neuras- 
thenia, trigeminal neuralgia, and locomotor ataxia. 



CYTODIAGNOSIS. 

Cytodiagnosis consists in a differential study of the cellular 
elements found in fluids recovered from the serous sacs (see differ- 
ential leukocyte count, p. 98). 

Clinical Significance. — An excess of lymphocytes (mono- 
nucleosis) is probably suggestive of tuberculosis or, more cor- 
rectly, indicative of the presence of foreign cells in the serous 
membrane, and that nature is endeavoring to eliminate such 
offending substance by means of the macrophagocytes, while a 
preponderance of polynuclear cells points toward suppurative 
processes or toward a widespread tuberculous or gummatous 
condition with probable necrotic change. Should the fluid 
contain many endothelial cells (endotheliosis), tuberculosis is to 
be favored. Polynucleosis is suggestive of a virulent infection 
(empyema), and is also to be found in such inflammatory mal- 
adies as rheumatism, malignancy, in heatstroke, and infarct of 

* "Zentralblatt fiir Innere Med.," Jan. 14, 1905. 



GASTRIC CONTENTS. 535 

the lung. In transudates, endothelial cells are found in sheets 
and clusters, and, according to Lewkowiez,* endotheliosis is sug- 
gestive of mechanical obstruction, as seen in transudates of heart 
and kidney disease. Vargas- Suarez found the eosinophils in- 
creased in cancer of the pleura and in two cases where the diag- 
nosis was obscure. There may be an excess of eosinophils in 
the blood, the cause of which is possibly dyspnea. In cancerous 
involvement of the serous surfaces one would expect to find many 
endothelial cells in the effusion from involved sacs. Erythrocy- 
tosis indicates a hemorrhagic process, and may depend upon a 
break in the continuity of the blood-vessels or upon an inflam- 
matory process. In two instances in which I recovered bloody 
fluid from the right pleura, the antemortem diagnosis and later 
the postmortem diagnosis was cirrhosis of the liver, the pleurae 
were normal. 

Transuded fluid will be found to contain a few leukocytes 
and endothelial cells, many of which show evidence of fatty 
degeneration. In ascitic fluid during the course of myelogenous 
leukemia many eosinophils and mast cells have been noted. In 
cases in which the fluid is concealed for a long time crystals of 
cholesterin and Charcot-Leyden crystals may be found, the former 
being oftenest found in hydrocele fluids. 

Cytodiagnosis oj Mumps. — Sicard and DopterJ collected 
saliva directly from the parotid gland by introducing a short 
piece of a fine sound through the excretory duct of the gland. 
The saliva from 32 persons free from mumps contained very 
few cells, but that from 52 persons with mumps was pathologic 
almost from the onset in 49 instances. By examining the saliva 
from the gland in this way it is easy to differentiate parotitis at 
any stage and to reveal the parotitic origin of certain affections 
of the testicles. 

Method. — I. Collect the fluid in a clean bottle and cork 
tightly until ready to begin its cytologic study. 

2. Place the fluid in the centrifuge or the torfuge and sediment 
for from three to ten minutes. 

3. Lift the sediment into a pipet and transfer it to a slide, 
where spread thinly over a comparatively large surface. 

4. Dry this preparation in the air and fix by heat or by the 
fumes of formalin (see Fixing Blood, page 74). 

5. Strain for one-half minute with a solution composed of one- 
half of I per cent, of eosin in 70 per cent, alcohol; and counter- 

*"Wien. klin. Woch.," Sept. 1904, p. qyS. 

t " Beitrage zur. klinik der Tuberkuk:)se," 1Q04, Bd. ii, p, 201. 

t"Presse Medicale," March 29, 1905. 



536 ADDENDA. 

stain with a 2 per cent, aqueous solution of methylene-blue, for 
one-half minute. Wash in water and study under a one-twelfth oil- 
immersion objective (see Differential Leukocyte Count, page 98). 

Caution. — Upon standing serous fluids often develop a floc- 
culent coagulum or sediments in which many of the cellular 
elements become entangled, hence cytologic examination of such 
fluids is valueless. 



EXUDATES. 

PARASITES OF SMALLPOX, VACCINIA, AND VARICELLA. 

It is quite well established that in the lymph of smallpox, 
varicella, and vaccinia are to be seen small unicellular bodies 
(protozoa) which possess a variable degree of ameboid movement. 

Parasite. — The organism is a spherical body 2-70 o- of ^.n 
inch in diameter, containing a rather large central nucleus. This 
nucleus is somewhat obscured by numerous refractile granules, 
which are regarded as probable spores. The extra-cellular spore- 
like bodies are motile unless found in glycerinated calf-lymph. 
The cytoplasm of the cell is finely granular. 

Detection. — i. Collect the lymph from the vesicles of the 
several diseases and study in a hanging-drop preparation (see 
Widal reaction, p. 118). 

2. Keep the specimen warmed at body-temperature and 
examine under a one-twelfth oil-immersion objective. 

Cautions. — In variola collect the lymph on or before the 
fifth day of the eruption. Human vaccine lymph should be 
procured upon the eighth or ninth day. The parasite of 
chickenpox is demonstrable in lymph gathered the first, second, 
and third days of the eruption, and is very motile, as is also the 
parasite of human vaccine. Dilute glycerinated calf-lymph to 
four times its bulk with normal saline solution. 

SEROUS EXUDATES. 

Protozoon of Scarlet Fever. — C. W. Duval,* in the study 
of 18 cases of scarlet fever, produced bHsters by the use of ammonia 
and examined their serum for protozoa-hke bodies (Mallory's. 
bodies). In five instances positive results were obtained, and in 
three of these the spherical segmented forms were observed. Posi- 
tive results were obtained when the eruption was fully developed. 

In one case that succumbed to the malady foci of organisms 

* "Univ. of Penn. Med. Bui.," Nov., 1904. 



EXUDATES. 537 

apparently identical with those detected in the serum of the 
blisters were found in the skin. 

CHYLOUS EXUDATES, 

DISTINCTIVE FEATURES OF CHYLOUS AND PSEUDOCHYLOUS 

FLUIDS. 

True Chylous Effusion. Pseudochylous Effusion. 

1. The fluid consists of a fine emul- i. A less perfect emulsion containing 

sion containing but few cellular large numbers of epithelial cells 

elements. and granular debris which is seen 

to display the various stages of 
degeneration, and to contain few 
fat droplets. 

2. Accumulates rapidly after tapping. 2. Collects more slowly, varying with 

the exciting pathologic cause. 

3. Contains sugar. 3. Sugar absent, as a rule. 

4. The melting-point of the fat pres- 4. Fatty foods have no effect on the 

ent in the fluid will be found to melting fats contained in the fluid, 

vary with the melting-point of the 
fat taken as food. 

5. The amount of fat present is in 5. Not affected by diet. 

direct relation with the amount 
of fats ingested. 

6. On standing a distinct creamy layer 6. A layer may collect which varies 

does not collect on the surface of with the number of oil droplets 

the liquid. present. A heavy sediment is lia- 

ble to collect at the bottom of the 
liquid. 

7. Fluid obtained by paracentesis may 7. Does not emit the odor of foods. 

emit the odor of foods that have 
been ingested. 

Clinical Significance. — Analysis of reports of 126 cases of 
milky ascites (2 cases observed personally) gave 24 complicating 
carcinoma; 17 cases resulting from tuberculosis; 11 cases accom- 
panying cardiovascular conditions; 8 cases due to disease of the 
liver; 7 cases following puerperal sepsis; and 4 cases the result 
of congenital cysts. 

In addition, there were 3 instances where chylous ascites fol- 
lowed infection with the filaria sanguinis hominis. Obstruction 
to the thoracic duct was observed postmortem in 11 of the cases, 
and the duct or receptaculum was found to be ruptured as the 
result of traumatism in 7 of the cases. 

Sixty-one of the cases were females, 50 males, and in the re- 
maining reports the sex was not given. A further analysis as to 
the number of cases occurring at the various periods in life gave 
6 under one year of age ; 3 between one and five years ; 1 3 between 
five and ten years; 9 between ten and twenty years; 12 between 
twenty and thirty years; 34 between thirty and fifty years; and 
24 after the age of fifty. 

Milky fluid is also met with in the pleural and pericardial sacs. 



538 ADDENDA. 



CYTOLOGIC STUDY OF SPINAL FLUID, 

Sicard, Widal, Ranout, and Wieder and Mamlock have con- 
tributed elaborate papers upon the chnical values of cytodiagnosis 
of the spinal fluid in diseases of the meninges, brain, and cord. 
These studies have even included the most varied affections of 
the nervous system, and the point of special interest appears to 
be an increase in the relative proportion of small mononuclear 
leukocytes (lymphocytes). The lymphocytes have been found 
increased in tabes, progressive paralysis, cerebrospinal syphilis, 
syphilitic hemiplegia, herpes zoster, and sciatica. The lympho- 
cytes are not increased in syringomyelia, poliomyelitis, polyneu- 
ritis, hemiplegia of old age, compression myelitis, functional neu- 
roses, epilepsy, and cerebral tumor. 

Cases of general paralysis, tabes and those of syphihtic origin 
provide the most constant findings (mononucleosis); but in 
these the findings are often confusing, giving an increase in the 
percentage of lymphocytes at one examination and a normal or 
decreased number at another. In uremia with convulsions a 
moderate increase in the mononuclear cells is common; while 
in tetanus the increase is likely to be more decided, and may be 
associated with many pol}Tnorphonuclear leukocytes. Brain 
tumor and tumor of the cervical cord have shown a decided in- 
crease in mononuclear cells. 

The number of contradictory statements regarding cytologic 
study of the spinal fluid makes it difficult for one to arrive at 
definite deductions. This diff'erence in the results obtained by 
different observers is dependent in part at least upon the varied 
technique employed, and also because there was no set schedule 
observed as being normal for the cerebrospinal fluid of man (see 
Differential Leukocyte Count, page 98). 

INDICAN IN THE URINE. 

The following test has proved very satisfactory in the hands of 
Dr. Daland: To 10 c.c. of filtered urine add one drop ol a i per 
cent, potassium chlorate solution, then 5 c.c. of chloroform, and, 
lastly, 10 c.c. of pure fuming hydrochloric acid (specific gravity 
1. 19). It is ver\^ necessary that the reagents should be added in the 
order given. 

Mix thoroughly by pouring repeatedly from one test-tube to 
another. By this method the indican (indoxyl-potassium-sulphate) 
is reduced to indigo which dissolves in the chloroform and imparts 
a blue color to it. In about ten minutes the maximum coloration 



INDICAN IN THE URINE. 539 

has been reached and the whole Hquid should again be thoroughly 
mixed. The chloroform will be colored more or less blue according 
to the amount of indigo set free. 

If the urine contains iodids, the chloroform will be colored vio- 
let. This violet color may be removed by adding three drops of a 
5 per cent, aqueous solution of sodium thiosulphate, whereupon the 
blue coloration, if present, will appear. 



NDEX. 



Abbe condenser in study of urine, 258 
Abortion, menstrual fluid after, 485 
Abscess, blood in, 137 

pulmonary, sputum in, 445 
Acetate of soda solution, 184 
Acetic acid fermentation, 343 
in feces, 368 
in urine, 250 
test for, 343 
Aceto-acetic acid in urine, 240 
Acetone in stomach , 348 

in urine, 240 
Acetonemia, blood in, 69 
Acetonuria, 240 

tests for, 241 
Achorion Schonleinii, 506 
Achromacyte, 89 
Achroodextrin, test for, 341 
Acid-fast bacilli, differentiation, 441 
Acid, leukocytosis from, 104 

urine, sediments in, 260 
Acidity of blood, 64 
Actinomyces in pus, 498 
in saliva, 458 
in sputum, 437 
in urine, 301 
Actinomycosis, blood in, 139 
fungi of, in sputum, 437 
of genito-urinary tract, 301 
pus of, 498 
saliva in, 458 
Acute infectious diseases, 133 
Addison's disease, blood in, 142 
Adenin in urine, 200 
Adjustment of focus, 24 

u'heel, 24 
Agamodistomum ophthalmobium, 473 
Agglutinin, 126 
Albumin in blood, 64 
in exudates, 488 
in saliva, 453 
in transudates, 488 
in urine, 206 
albuminonieter for estimating, 212 
Boston's test for, 207 
clinical significance of, 527 
Douglas' test, 206 
Esbach's estimation, 211 
estimation, 211 
globulin and, separation, 206 
gravimetric estimation, 213 
heat in estimation, 211 
Ravold's test, 526 
reaction ring in Boston's test, 209 
tests for, 206 

volumetric estimation, 211 
nucleo-. See Mucin. 
serum-, in sputum, 451 
Albuminoids, gastric digestion of, 341 
Albuminometer, Esbach's, 212 
Albuminous expectoration, color of, 430 
Albuminuria, 206 

emulsion-, 216 
Albumose, Bence-Jones', 21S 



Albumose in urine, Boston's test for, 210 

Millon's test for, 217 
Alcohol and phosphates in urhie, 182, 183 
glucosuria after, 225 
leukocytosis from, 104 
Alcoholic ether, 202 
Alkaline hematoporphyrin, 223 
urine, amorphous deposits in, 277 
sediments in, 260, 275 
Alkalinity of blood, 60 

Dare's hemoalkalimeter for, 61 
estimation of, 61 

Lowy's method of estimation, 61 
Alkalis, leukocytosis from, 104 
Alkaloids in urine, 256 
Alkaptonuria, 247 
fermentation test for, 247 
Garrod's test for, 247 
phenylhydrazin test for, 247 
pokirimetry for, 247 
AUoxur bases, 106, 200 
Almen's solution, 215 
Aloin test for blood, 355 
Ameboid movements of red cells, 90 
American fluke, large, 413 
Ammonia, electric conductivity of, 175 
in stomach, 349 
in urine, 177, 246 
Ammoniacal magnesium mixture, 199 
Ammoniomagnesium phosphates in urine, 271 
Ammonium urate in alkaline urine, 276 
Amoeba coli, blood-cells in, 392 
in feces, 388 
in pus, 497 
in sputum, 436 
histolytica, 389 
urogenitalis in urine, 300 
Amorphous deposits in urine, 274 

alkaline, 277 
Amyl nitrite, glucosuria after, 225 
Amyloid casts in urine, 2S9 
Anchlorhydria, 326 
Anchylostoma, See Uncinaria. 
Anemia, 82 
chlorotic type, 127. See also Chlorosis. 
pernicious, 126. S^QaXsoPemicioits anemia. 
primary, 82 
quantitative, 94 
secondary, 82, 88 
ameboid motion iti, 90 
blood in, 88 

Brownian movements in, 90 
crenation in, 90 
decoloration of blood in, 89 
differential diagnosis, 12S 
dwarf-cells in, 90 
Eichhorst's corpuscles in, 90 
endoglobular changes in blood in, 89 
macrocytes in, 92 
megaloblasts in, 92 
megalocytes in, 90 
miorocytes in, 90 
motilitv of red cells in,8Q 
necrosis of red cells in, 92 



541 



542 



INDEX. 



Anemia, secondary, poikilocytosis in, 89 
red cells in, 89, 92 
rouleaux formation in, 88 
schistocytes in, 90 
shape of red cells in, 89 
size of red cells in, 89 
viscosity of blood in, 88 
splenic, 132 
Anesthesia, leukocytosis of, 102 

polycythemia from, 85 
Angina, ulcerative stomatitis with, saliva in, 

455 
Anguillula aceti in urine, 298 

stercorals in blood, 143 
Anhydremia, blood in, 83 
Anilin-gentian-violet for tubercle bacilli, 440 
Animal gum in urine, 239 
inoculation with blood, 110 
parasites in feces, 383. See also Intestinal 
parasites. 
in pus, 497 
in urine, 292 

Stiles' key to, 299 
in vaginal secretion, 484 
of lung, 435 
Anise-seed oil, leukocytosis from, 103 
Ankylostoma. See Uncinaria. 
Ankylostomiasis, 415 
Anthracosis, sputum in, 449 
Anthracotic sputum, 430 
Anthrax bacillus in pus, 497 
bacteria in blood in, iii 
blood in, 139 
Antifebrin in urine, 256 

sulphates in urine and, 185 
Antimony in urine, 256 

leukocytosis from, 104 
Antipyrin, color of urine and, 171 
in urine, 256 
leukocytosis from, 104 
Antistreptocolysin, 118 
Anuria, 169 
physiologic, 169 
toxic, 169 
Appendicitis, blood in, 137 
Arabinose in urine, 238 
Arnold's test for diacetic acid, 243 
Arsenic, glucosuria after, 225 
in urine, 256 
leukocytosis from, 104 
Arthritis, intermittent glucosuria of, 226 
Articular rheumatism, acetonuria in, 242 
Artificial light for microscope, 18 
Ascaris canis, 414 

in nasal secretion, 467 
in sputum, 437 
lumbricoides, 414 
in blood, 143 
in urine, 297 
mystax, 414 
Aspergillosis, fungi of, in sputum, 437 
Aspergillus fumigatus in sputum, 437 
in urine, 301 

pneumomycosis and, 437 
in sputum, 437 
in urine, 301 

niger in ear discharge, 469 
in sputum, 437 
Aspiration with stomach-tube, 313 
Asthma, acetonuria and, 242 

bronchial, sputum in, 445 
Auditory canal, discharges from, 468 

larvae in discharges from, 470 
Axial light, 18 
Azoosnermism, 480 



Bacilli, acid-fast, differentiation, 441 
Bacillus coli communis in urine, 307 
colon, Widal reaction and, 124 



Bacillus dysentericus, Widal reaction and, 

124 
febris gastrica, Widal reaction and, 124 
fusiform in saliva, 455, 456 
grass, Moeller's, tubercle bacillus and, dif- 
ferentiation, 441 
Klebs-Loffler, in sputum, 442 
Koch-Weeks', 475 
lepra. See Bacillus of leprosy. 
ma'lei, diseases found in, 516 

"n nasal secretion, 466 

m pus, 497 

Widal reaction and, 125 
mesentericus, Widal reaction and, 124 
of anthrax in pus, 497 
of Boas-Oppler in gastric fluid, 350 
of bubonic plague, Widal reaction and, 124 
of butter, tubercle bacillus and, differentia- 
tion, 441 
of Doderlein in vaginal secretion, 481 
of dysentery, 381 
of Friedlander in nasal secretion, 467 

in sputum, 445 
of glanders, diseases found in, 516 

in pus, 497 

Widal reaction and, 125 
of influenza in sputum, 443 
of leprosy, Bacillus tuberculosis and, dif- 
ferentiation, 441 

in blood, 140 

in nasal secretion, 467 

in pus, 497 
of ozena, 467 
of Shiga, 381 

of smegma. Bacillus tuberculosis and, dif- 
ferentiation, 441 
of tetanus in pus, 497 
of typhoid. See Bacillus typhosus. 
of Vincent in saliva, 455, 456 
plague, Widal reaction and, 124 
proteus vulgaris in urine, 307 

Widal reaction and, 125 
pyocyaneus, green urine from, 170 

in urine, 307 

Widal reaction and, 125 
subtilis in gastric fluid, 350 
tuberculosis, anilin-gentian-violet for, 440 

butter bacillus and, differentiation, 441 

diseases found in, 516 

in feces, 380 

in milk, 519 

in nasal secretion, 466 

in pus, 494 

in sputum, 438-442 
in anthracosis, 449 

in urine, 303, 307 

lepra bacillus and, differentiation, 441 

Moeller's grass bacillus and, differentia- 
tion, 441 

smegma bacillus and, differentiation, 441 



Widal reaction and 
^phosus cult! 
in feces, 381 



typhosus culture, for Widal reaction, 119 



/idal 



m nasal secretion, 467 
in urine, 305 

Widal reaction for, 118. See also Widal 
reaction in typhoid. 
Bacteremia, 107 
Bacteria in blood, iii, 115 
reaction of, 108 
in bone-marrow, 115,116 
in feces. 380 
in gastric contents, 350 
in milk, 519 
in saliva, 454 
in semen, 480 
in sputum, 438 
in urine, 301, 302 
in vaginal secretion, 481, 482 
Bacteriology of blood, 107 



INDEX. 



543 



Bacteriuria, 301 
Bail's test for pentosuria, 238 
Balantidium coli in feces, 395 
in pus, 497 
in sputum, 436 
Barber's itch, 509 
Barford's reagent, 342 
Barium-chlorid mixture, 191 
Basic capacity of blood, 64 
Basophilia, granular, 91 
Basophils in myeloid leukemia, 131 

polynuclear, 96 
Baths and phosphates in urine, 182, 183 
Beakers, nest of, 184 
Beef tape-worm, 399 

in blood, 147 
Belladonna, leukocytosis from, 104 
Bence-Jones' albumose, 218 

Boston's test for, 187, 188 
Bicarbonate of soda, leukocytosis from, 104 
Bile acids in urine, 239 

in gastric contents, 351 

in urine, 239 

in vomit, 354 
Bilharzia haematobia, eosinophilia from, 106 
in blood, 147 
in sputum, 436 
Biliary acids in blood, 69 
in blood serum, 69 
in feces, 368 

calculi in feces, 376 

coloring matter, green urine from, 170 

urine, 239 
Bilious stools, color of, 361 
Bilirubin crystals in urine, 270 

in blood, 69 
Biliuria, Boston's test for, 210 
Bismuth, color of stools and, 361 

leukocytosis from, 104 

sulphid crystals in feces, 380 
Biuret reaction, with peptones, 217 

test for peptic digestion, 340 
Black sputum, 430 
Blastomycetes, 512 

in blood, 114 
Blastomycetic dermatitis, 512 
Blastomycosis, 512 

Blennorrhea, vaginal, secretion in, 486 
Blood, 30 

acidity of, 64 

albumins in, 64 

alkalinity of, 60 

Dare's hemoalkalimeter for, 61 
estimation of, 61 
Lowy's estimation, 61 

aloin test for, 355 

altitude and, 86 

Anguillula stercoralis in, 143 

animal inoculation with, no 

Ankylostoma duodenale in, 143 

Ascaris lumbricoides in, 143 

bacteria in, 108, 111-115 

bacteriology of, 107 

basic capacity of, 64 

beef tape-worm in, 147 

Bilharzia haematobium in, 147 

biliary acids in, 69 

bilirubin in, 69 

blastomycetes in, 114 

Cabot's ring-bodies in, 91 

centrifugalizing, 38-40 

character of, 37 

coagulation time, 41 

collection, 33 
for bacteriologic study, 109 
for Widal reaction, 118 

color of, 46 

colorimetry of, 46 

corpuscles of, red. See Red corpuscles. 
white. See Leukocytes. 



Blood, cover-glass preparations, fixing, 74 
crescentic bodies in, 162 
cryoscopy of, 70 
cultures, 109 

Dare's hemoglobinometer for, 46 
decoloration of, in secondary anemia, 89 
degenerated leukocytes in, 98 
diastatic ferment of, 70 
Distoma haematobium in, 147 
Dracunculus medinensis in, 149 
dust, 100 

Eichhorst's corpuscles in, 90 
endoglobular changes in, in secondary 

anemia, 89 
examination, immediate, 34 

schedule of, 144 

spectroscopic, 43 
fat in, 66 
fatty acids in, 66 
fermentative power of, 70 
fibrinogen in, 64 
films, no 
fixing, 74 
fluke, bovine, 146 

human, 146 
for hemocytometer, 52 
fresh, study of, 32 
fungi in, 114 
glucose in, 67 
glycogen in, 65 
guaiacum test for, 31 
hemoglobin in, 64 
hyaline bodies in, 159 
hyperviscosity of, 88 
hypoviscosity of, 89 
icteric, 69 
in feces, 360, 372 

in sputum in tuberculosis, 447, 448 
in stools, 360, 372 

in urine, 221, 281. See also Hematuria. 
in vomit, 354 

inoculation with, animal, no 
inorganic substances in, 65 
isotonic tension of, toxins and, 108 
lepra bacillus in, 140 
lymphoid, 131 
macrocytes in, 90 
malarial parasite in, 157. See &\?,o Malarial 

parasite. 
megaloblasts in, 92 
megalocytes in, 90 
microblasts in, 94 
microcytes in, 90 
microscopic examination, 37, 77 
myelocj'tes in, 97 
neutrophils in, transitional, 98 
normoblasts in, 93 
olein in, 66 
osmosis of, 73 
oval bodies in, 162 
Oxyuris vermicularis in, 143 
palmitin in, 66 
parasitic diseases of, 143 
pathology of, special, 126 
peptone in, 64 
pigmented bodies in, 159 

extracellular, 162 
Plasmodium malarise in, 157. See also 

Malarial parasite. 
pork tape-worm in, 147 
prothromhi in, 64 

red corpuscles of. See Red corpuscles. 
reports, clinical, 33 
segmenting bodies in. 160 
serum, biliar\- acids in, 6q 

glohulicidal properties of, 70 

toxicity of, 70 
serum-albumin in, 164 
serum-globulin in, 64 
slides, fixing, 74 



544 



INDEX. 



Blood slides, mounting, 80 
smears, 35 

special pathology of, 126 
specific gravity of, 40 

hemoglobin and, 40 
spectra of, 43 
spheric bodies in, 162 
stained, study of , 74, 77, 78 
stains for, 76, no. See also Stains for 

blood. 
stearin in, 66 

Strongyloides intestinalis in, 143 
suppurative organisms in, 113, 114 
Taenia saginata in, 147 
Teichmann's test for, 31 
tests for, 31 

transitional neutrophils in, 98 
Trichina spiralis in, 146 
Trichocephalus dispar in, 143 
trypanosoma in, 152 
Tiirck's stimulating forms in, 98 
Uncinaria duodenale in, 143 
urea in, 65 
uric acid in, 65 
viscosity of, 8g 
volume of, 31 
Blood-casts in urine, 284, 287 
Blood-cells, life of, 37 
Blood-corpuscles, counting, 52, 54 
Oliver's hemocytometer, 58 
Thoma-Zeiss instrument, 52 
in feces, 375 

red. See Red corpuscles. 
Thoma-Zeiss method of counting, 52 
white. See Leukocytes. 
Blood-lancet, Daland's, 34 
Blood-plates, 100 
Bloody sputum, 430 
urine, 170 
parasites in, 297 
Blotting-paper test for hook-worms in feces, 

387 
Blue-bottle fly in feces, 411 
Boas' aspirator, 309, 310, 313 
estimation of pepsinogen, 337 
test for lactic acid, 346 
test-breakfast, 316 
Boas-Ewald's test-breakfast, 315 
Boas-Oppler bacillus in gastric fluid, 350 
Body fluids, Widal reaction with, 123 
Bone-marrow, bacteria in, 115, 116 

extract, leukocytosis from, 104 
Boric acid crystals in urine, 267 
Boston's method for specific gravity of milk, 
520 
for sulphur in urine, 187, 188 
for Bence-Jones' albumose, 187, 188 
slide and cover-glass forceps, 439 
test for albumin, 207 

reaction ring in, 208, 210 
for albumose, 210 
for biliuria, 210 
for globulin, 210 
for indican, 211 
for mucin, 210 
for imcleo-albumin, 210 
for peptones, 210 
for resinous bodies in urine, 211 
for urates, 210 
for urinary pigments, 210 
Bothriocephalus latus infection, blood in, 147 

jiguloides in urine, 300 
Bottger's test for glucosuria, 229 
Bovine blood fluke, 146 
Breath, moisture of, 533 

Bromid of potassium, alkaline phosphates in 
urine and, 182 
sulphates in urine and, 185 
Bromin in urine, 256 
Bronchial asthma, sputum in, 445 



Bronchitis, sputum in, 443, 444, 446 
Bronchopneumonia, sputum in, 445 
Bronchorrhea, 444 
Brownian movements in secondary anemia, 

Browning s spectroscope, 43, 44 
Bubonic plague, bacteria in blood in, 114 

blood in, 139 

nasal secretion in 467 

Widal raaction in, 124 
Buccal secretion, 452. See also Saliva. - 

clinical significance in disease, 534 
Buret, 181 
Burns, blood in, 85 

Butter bacillus and tubercle bacillus, 441 
Butyric acid in feces, 368 * 

in gastric contents, source, 342 

in urine, 250 

test for, 343 



Cabot's ring-bodies, 91 
Cadaverin in urine, 254 
Caffein, glucosuria after, 225 

leukocytosis from, 104 
Cahn-Mehring method for estimating fatty 

aicids, McNaught's modification, 343 
Calcium carbonate in urine, 277 

oxalate in urine, 265 
amorphous, in urine, 274 

phosphate in feces, 379 
in urine, 182, 267 

soap in urine, 266 

sulphate, amorphous, in urine, 274 
cryst?ls in urine, 266 

urate, acid, amorphous, in urine, 275 
Calculi in feces, 376 
Calomel, color of stools and, 361 
Camerer's estimation of purin in urine, 529 
Cammidge's reaction, 531 
Camphor, eosinophilia from, 107 

leukocytosis from, 103 
Cancer fragments in urine, 291 
Carbohydrates, digestion of, 341 

in urine, 224 
Carbolic acid, brown urine from, 170 
in urine, 256 
leukocytosis from, 104 
Carbolic-acid gas in urine, 254 
Carbol-thionin for malarial parasite, 158 
Carbon dioxid in feces, 364 

in stomach, 349 

monoxid, glucosuria after, 225 
Carbonate of lime in urine, 277 
Carbonate-of-silver test for uric acid, 197 
Carbonic-oxid poisoning, polycythemia from, 
88 

hemoglobin, 43 
spectrum of, 45 
tests for, corroborative, 45 
Carcinoma, gastric, acetonuria in, 242 

of cervix, 484 
Casein, human, 518 
Caseous panicles in sputum, 431 
Castor oil, leukocytosis from, 104 
Casts in feces, 373 

in urine, 283. S&q sXso Renal casts. 
Catheterization for bacteriologic study, 301 
Cause's test for glucosuria, 233 
Caustic potash, leukocytosis from, 104 
Centigrade, Fahrenheit equivalents for, 526 
Centimeters, inch equivalents, 526 
Centrifugal analysis of urine, 189 

estimation of chlorids in urine, 189 
of phosphates in urine, 190 
of sulphates in urine, 191 
Centrifuge, electric, with rheostat, 38 

for urine, 257 

hand, 38, 39 

percentage tube for, 189 



INDEX. 



545 



Centrifuge, Purdy's tubes for, 189 

sediment tube for, 189 

water-motor, 189 
Cercomoiias hominis, 394 

in feces, 392 

intestinalis, 394 
Cerebral depressants, alkaline phosphates in 

urine and, 182 
Cerebrospinal fluid, 500 

Diplococcus intracellularis in, 502 
in nasal secretion, 466 
staining, 502 
. meningitis, diplococcus of, 502 

bacteria in blood in, 114 
Cervix, carcinoma of, 484 

ulceration of, 484 
Cestodes, 396. See also Tape-worm. 
Chalicosis, sputum in, 450 
Charcot-L eyden asthma crystals, 445, 446 

crystals in feces, 379 
in myeloid blood, 131 
in nasal secretion, 467 
in semen, 478 
in sputum, 433 
Chestnut-burr crystals, 272, 276 
Chionyphe Carteri, 513 
Chloral, alkaline phosphates in urine and, 182 

glucosuria after, 225 

leukocytosis from, 104 
Chlorid-of-barium mixture, 191 
Chlorids in urine, 179 

centrifugal estimation, 189 
phosphates and urea and, ratio, 193 
Chloroform, acetoimria and, 242 

alkaline phosphates in urine and, 182 

leukocytosis from, 103 
Chlorophyl in feces, 372 
Chlorosis, 127 
Cholalic acid in feces, 368 
Cholemia, blood in, 69 

isotonic tension in, 69 
Cholera, Widal reaction in, 124 
Cholesterin crystals, 245 
in feces, 370, 379 
in urine, 245, 272 
Chrysomyia mascellaria, 513 
C'hyle in urine, 253 
Chyloid exudates, 493 
Chylous exudates, 493 

clinical significance of, 537 

urine, 252 
Chyluria, 252 

color of urine in, 170 

parasitic, 253 
Chymosin, 338 

hydrochloric acid and, 338 
Chymosinogen, 339, 340 
Cigar crystals, 264 

Cipollino's test for hydrochloric acid, 533 
Clap shreds in urine, 291 
Clinical blood reports, 33 
Coagulation time of blood, 41 
Coagulometer, Bifli's, 523 
Coagulometer, Wrighi's, 141 
Coal-dust in sputum, 449 
Coating of tongue, 458 

Cocain, alkaline phosphates in urine and, 183 
Coccidiosis, intestinal, 388 
CoccSdium bigeminum, 388 
Cochin-China diarrhea worm, 421 
Cod-liver oil, lipuria after, 252 
Cold-baths and phosphates in urine, 183 
Collagen, digestion of, 341 
Colon bacillus in urine, 306, 307 

Widal reaction and, 124 
Colorimetry of blood, 46 
Colostrum, 517 

corpuscles, 518 
Combined iiydrochloric acid in gastric con- 
tents, 333 

35 



Composite casts in urine, 284, 289 
Concretions, urinary, 278 

in feces, 376, 377 
Condenser of microscope, 25 
Congo-red test for free hydrochloric acid, 330 

test-paper for acidity of gastric contents, 322 
Conjugate sulphates in urine, estimation of, 

187 
Conjunctiva, secretion from, 470 
Conjunctivitis, acute infectious, 475 

diphtheric, 474 

gonorrheal, 470 
Constipation, 358 

pathologic, 357 
Copper test for glucosuria, 226 

for uric acid, 197 
Cornea, abscess of, 474 

inflammation of, discharge from, 471 
Corpuscles, blood-. See Blood-corpuscles. 

colostrum, 518 

Eichhorst's, 90 

in feces, 375 

red. See Red corpuscles. 

salivary, 454 

white. See Leukocytes. 
Corrosive sublimate, leukocytosis from, 104 
Counting chamber of Thoma-Zeiss hemocy- 

tometer, 54 
Cover-glass and slide forceps, Boston's, 439 
Cover-glasses, 32, 34 

blood, fixing, 74 

surrounding of, with cement, 28 
Cow and human milk, 518 
Crenation in secondary anemia, 90 
Crescentic bodies in malaria, 162 
Cresol in feces, 365 
Crocker's method to detect Tinea versicolor, 

5" 
Croton oil, leukocytosis from, 104 
Cryoscopy of blood, 70 

of urine, 72 
Cultures, blood, 109 

for Widal reaction, 119 

from saliva, 455, 461 

from synovial fluid, 504 

from throat, 461 

in bacteriuria, 302 
Culture-tubes, inoculation of, 463 
Cupric tartrate, alkaline solution of, 227 
Curschmaim's spirals in sputum, 433 
Cyanosis, blood in, 84 
Cylindroids in urine, 284, 290 
Cyst, hydatid, fluid of, 491 

of eyelids, parasitic, 476 

ovarian, 490 

pancreatic, fluid of, 491 

renal, 490 
Cystic fluids, 488 

fixing sediment, 489 

sedimentation, 489 

staining sediment, 489 

Cysticercus cellulosa;, 399 

Cystin crystals in urine, 271 

green urine from, 170, 246 
Cystinuria, 170, 246 
Cystitis, bacteriuria in, 307 

purulent, blood in, 137 
Cytodiagnosis, 490, 534 

of spinal fluid, 538 



Daland's armature of centrifuge, 30 

blood-lancet, 34 
Dare's hemoalkalimeter, 61 

heinuglobini>meter, 40 
Dark bodies in urine, 274 
Degeneration, punctate basic, of red cells, oi 
Degree of acidity, 323 
Demodex foUiculorum, 476 
Dern\acentor reticulatus, 15s 



V. 



546 



INDEX. 



Dermatitis, blastomycetic, 512 

mycotic, 510 

protozoic, 512 
Dermatobia noxialis, 514 
Desiccator, 178 
Dextrin in urine, 239 
Dextrose, Barford's reagent for, 342 

in urine, 224. See also Gliicosuria. 

test for, 341 
Dhobie itch, 510 
Diabetes, acetonuria and, 241 

blood in, 68 

mellitus, 224. See also Glucosuria. 

phosphatic, 182 
Diacetic acid in urine, 243 
Diaceturia, 243 
Diaphragm of microscope, 17 

iris, 17 
Diarrhea, 358 

worm, Cochin-China, 421 
Diastatic ferment in saliva, 453 

of blood, 70 
Diazo-reaction, Ehrlich, 249 
Dibothriocephalus latus, 402 
Dicroccelium lanceatum, 412 
Differential density test for glucosuria, 235 
Digestion, gastric. See Gastric digestion. 
Dihydroxyphenylacetic acid in urine, 247 
Dimethylamido-azobenzol for free hydro- 
chloric acid, 328 
Dimethylamidobenzaldehyd reaction, Ehr- 

lich's, 249 
Diphtheria bacillus in sputum, 442 

bacteria in bone-marrow in, 116 

bacteriuria in, 306 

blood in, 135 

diagnosis, outfit for, 462 

of vulva, 484 

tonsillar membrane in, 459 
Diphtheric conjunctivitis, 474 
Diplobacillus, Morax-Axenfeld, 475 
Diplococcus intracellularis in cerebrospinal 
fluid, 502 
in nasal secretion, 466 

scarlatinae in urine, 306 
Dipylidium caninum, 407 
Distilling apparatus, 365 
Distoma haematobium in blood, 147 
in urine, 295 

pulmonale, 435 

ringed, 435 

sinense, 413 
Diuretin, glucosuria after, 225 
Doderlein bacillus in vaginal secretion, 481 
Dog tape-worm, 400, 406 
double-pored, 407 
small, 404 
Doremus ureometer, 194 

Hinds' modification, 194 
Douglas' method for albumin in urine, 206 
Dourine, 151 
Dracontiasis, 149 
Dracunculus medinensis, 149 
Drepanidium, 157 

ranarum, 155, 157 
Drugs, effect on urine, 255 

leukocytosis after, 103 
Dumb-bell crystals, 276 
Dum-dum fever, 167 
Dwarf cells, 90 

tape-worm, 406, 407 
Dysentery bacillus, 381 
in feces, 381 

Widal reaction in, 124 
Dysmenorrhea, discharge in, 486 



Ear discharges, 468 
Echinococcus cysts in urine, 292 
in pus, 497 



Echinococcus polymorphus, 404 
Ectozoa, classification, 386 
Eczema, 515 

Edema of lung, sputum in, 448 
Egyptian fluke, 412 

strongyle, 421 
Ehrlich diazo-reaction, 249 

dimethylamidobenzaldehyd reaction, 249 

tricolor mixture, 79 
Eichhorst's corpuscles, 90 
Eimeria bigemina, 388 
Einhorn's capsules, 314 

saccharimeter, 230 
Elastic fibers in sputum, 434 
Elastin, digestion of, 341 
Electric centrifuge with rheostat, 38 
Elephantiasis, non-parasitic, 153 
Emulsion in albuminuria, 216 
Endemic hemoptysis, 435 
Endocarditis, gonorrheal, bacteria in blood 
in, 114 
gonococci in blood in, 114 

ulcerative, bacteria in blood in, 114 

bacteriuria in, 304 
Endogenous purins, 523 
English and metric systems, relations, 526 

measures, 526 

weights, 526 
Entamoeba coli, 3S9 

histolytica, 389 
Entozoa, classification, 384 

in nasal secretion, 467 
Eosin and hematoxylin, 76, 77 

and methylene-blue for malarial parasite, 
158 
Eosinophiles, increase in, 105 
Eosinophilia, 105-107 

in scarlet fever, 135 
Eosinophilic myelocytes, 97 
Eosinophils, 94, 96, 105, 107 

in myeloid leukemia, 131 
Epidemic meningitis, bacteria in blood in, 
114 
diplococcus of, 502 
Epilepsy, acetonuria in, 242 

parasite in feces in, 410 
Epithelia in feces, 374 

in saliva, 454 

in sputum, 433 

in urinary sediments, 279 
features, 282 
Epithelial casts in urine, 288 
Eristalis, 410 
Erlenmeyer flask, 347 
Erysipelas, 515 

bacteria in bone-marrow in, 116 

bacteriuria in, 306 

blood in, 138 
Erythrasma, 512 

Erythrocytes, 81. See also Red corpuscles. 
Erythrodextrin, test for, 341 
Esbach's albuminometer, 42 

estimation of albumin in urine, 211 

reagent, 522 
Estivo-autumnal fever, 160 
hyaline bodies in, 159 
parasite of, 161, 165. Se& aXso Estivo-au' 

tumnal parasite. 
pigmented bodies in, 159 

parasite, 161, 165 

flagellation of, 165, 166 
staining, 158 
Ether, alcoholic, 202 

glucosuria after, 225 

leukocytosis from, 102 

ozonic, 222 
Ethereal sulphates in urine, estimation, 187 
Euchlorhydria, 326 
Eustrongylus gigas in urine, 299 
Ewald-Boas' test-breakfast, 315 



INDEX. 



547 



Ewald-Sievers' test of motor power of stom- 
ach, 318 
Exogenous purins, 523 
External auditory canal, discharge of, 469 
Exudates, 4S7, 492 

albumin in, 488 

chyloid, 493 

chylous, 493 
clinical significance of, 537 

fixing sediment, 489 

hemorrhagic, 493 

purulent, 493. See also Pus. 

sedimentation, 489 

seropurulent, 492 

serous, 492 

staining sediment, 489 
Eye, discharges from, 470 

trematodes of, 472 
Eyelids, parasitic cysts of, 476 
Eye-piece micrometer, 27 



Fahrenheit, centigrade equivalents for, 

526 
False casts in urine, 284, 290 
Fasciola hepatica,4ii 

^gyptiaca, 412 

angusta, 412 
magna, 413 
Fat, digestion of, 342 
in blood, 66 
in feces, 378 
in milk, estimation, 521 
in urinary sediment, 274 
in urine, 251 
Fatty acids, 342 

in blood, 66 

in feces, 367 

in gastric contents, 342 

in sputum, 451 

in urine, volatile, 250 
Fatty-acid casts in urine, 289 

crystals in feces, 378 
Favus, 506 
Fecal vomit, 354 
Feces, 356 
acetic acid in, 368 
after hemorrhage, color of, 360 
American fluke in, 413 
Amoeba coli in, 388 
Anguillula intestinalis in, 422 
animal parasites in, 383. See also Intesti- 
nal parasites. 
Ascaris canis in, 414 

lumbricoides in, 414 

mystax in, 414 
bacillus of dysentery in, 381 

of Shiga in, 381 

tuberculosis in, 380 

typhosus in, 381 
bacteria in, 380 
Balantidium coli in, 395 
biliary acids in, 368 

concretions in, 376 
bismuth and, 361 

sulphid crystals in, 380 
blood in, 360, 372 
blood-corpuscles in, 375 
blue-bottle fly in, 411 
butyric acid in, 368 
calcium phosphate in, 379 
calculi in, 376 
calomel and, odor, 361 
carbon dioxid in, 364 
casts in, 373 
cercomonas in, 392 

hominis in, 394 

intestinalis in, 394 
cestodes in, 396. See also Tape-worms. 
character, 357 



Feces, Charcot-Leyden crystals in, 378 
chemistry of, 362 
chlorophyl in, 372 
cholalic acid in, 368 
cholesterin in, 370, 379 
clay-colored, 361 
coccidia in, 3S8 
color of, 360 
coloring-matter in, 364 
composition of, 363 
concretions in, 376 
cresol in, 365 
crystals in, 378 

decomposition products in, 364 
Dicrocoelium lanceatum in, 412 
Distoma sinense in, 413 
drugs and, 361 
dysentery bacillus in, 381 
Egyptian fluke in, 412 

strongyle in, 421 
epithelia in, 374 
Fasciola hepatica in, 411 

^gyptiaca in, 412 

angusta in, 412 
magna in, 413 
fat in, 378 
fatty, 378 

acids in, 367 
fatty-acid crystals in, 378 
flagellata in, 392 
flukes in, 411 
food particles in, 371 
formic acid in, 367 
gall-stones in, 376 
gases in, 364 
glycocholic acid in, 368 
goblet cells in, 375 
green, 361 
helophilus in, 410 
hematoidin crystals in, 375, 379 
hook-worm in, 415 
hydrobilirubin in, 369 
hydrogen in, 364 
in biliousness, 361 
in constipation, 357, 358 
in diarrhea, 357 
in hook-worm infection, 386 
indigestible matter in, 363 
indol in, 365, 366 
intestinal calculi in, 376, 377 

l)arasites in, 383. See also hitestinai 
parasites. 

sand in, 377 
ipecac and, 361 
iron and, 361 

Japanese strongyle in, 421 
Lamblia duodenalis in, 394 
lancet fluke in, 412 
leukocytes in, 375 
liver fluke in, 411 
Egyptian, 412 
narrow, 412 
macroscopic constituents, 371 
manganese dioxid and, 361 
mastigophora in, 392 
metabolic products in, 364 
methane in, 364 
Megastoma entericum in, 394 
microscopic constituents of, 371 
mucoid, 372 
mucus in, 372 
Musca voniitoria in, 411 
nitrogen in, 364 
odor^ 359 

Opislhorcis sinense in, 413 
Oxyuris vermicularis in, 414 
Paramcecium coli in, 305 
parasites in, animal, 3S3, 401.). See also In- 
testinal parasites. 
phenol in, 365, 366 



548 



INDEX. 



Feces, phosphates in, 379 

pigments of, 369 

propionic acid in, 368 

purin bodies in, 533 

pus in, 376 

pus-producing organisms in, 381 

reaction of, 362 

red, 361 
corpuscles in, 375 

rhizopoda in, 3S8 

round-worm in, 414 

sand in, intestinal, 377 

santonin and, 361 

senna and, 361 

serum in, 372 

Shiga bacillus in. 3S1 

skatol in, 365, 366 

staphylococci in, 3S1 

starch in, 372 

stercobilin in, 369 

streptococci in, 381 

strongyloides in, 419, 422 

sulphid of bismuth in, 380 

tape-worms in, 396. See also Tape-worms. 

taurocholic acid in, 368 

tetramitina in, 392 

trematodes in, 411 

Trichinella spiralis in, 422 

Trichocephalus dispar in, 418 
hominis in, 418 

trichomonas in, 393 

triple phosphate in, 379 

tubercle bacillus in, 380 

typhoid bacillus in, 381 

tyrosin in, 365 

unassimilated food in, 363 

Uncinaria ankylostoma in, 415 

valerianic acid in, 368 

washing, 387 
Fehleisen's Streptococcus pyogenes, diseases 

found in, 516 
Fehling's solutions, 227, 232 

test for glycosuria, 227, 232 
Fermentation test for alkaptonuria, 247 

for glucose in urine, 230 
Ferments, 335 

in blood, diastatic, 70 

in saliva, 453 

in sputum, 451 

zymogens of", 335 
Feser's lactoscope. 521 
Fever, acetonuria in, 242 

eosinophilia in, 107 
Fibrin in urine, 224 
Fibrinogen in blood, 64 
Ficker's typhoid reaction, 525 
Filaria, 148 

Demarquaii, 148 

diurna, 147 

nocturna, 147 

perstans, 147 

sanguinis hominis, 147 
in pus, 497 
in sputum, 437 
in urine, 294 

spinal trypanosomiasis and, 148 

staining of, 148 
Filariasis, blood in, 147 

eosinophilia from, 106 
Films, blood, no 
Fish tape-worm, 402 
Fistulous secretions, 491 
Fixed blood, study of, 74 
Fixing blood combined with staining, 77 
Flagella of malarial parasite, 162 

function of, 166 
Flagellata in feces, 392 
Flat-iron crystals, 264 
Floaters in urine, 291 
Fluids, freezing-point of, 70 



Fluke, 411 

American large, 413 

bovine blood, 146 

Egyptian, 412 

human blood, 146 

lancet, 412 

liver, 413, 412 
Fly, blue-bottle, in feces, 411 
Focus, 22 

for urinary sediments, 258 
Focusing, 22, 24 
Foot-ball impetigo, 514 

Forceps, slide and cover-glass, Boston's, 439 
Formic acid in feces, 367 

in urine, 250 
Fraunhofer's lines in blood spectra, 44 
Free hydrochloric acid. See Hydrochloric 

acid in gastiic contents. 
Freezing-point of fluids, 70 
Fresh blood, study of, 32 
Friedlander's bacillus in nasal secretion, 467 

in sputum, 445 
Fungi in blood, 114 

in nasal secretion, 467 

in pus, 498 

in sali\a, 454, 457 

in sputum, 437 

in urine, 300 

in vaginal secretion, 486 

Widal reaction and, 125 
Fusiform bacillus in saliva, 455, 456 



Gabbett's methylene-blue solution, 439 
Gall-stones in feces, 376 
Gangrene, pulmonary, sputum in, 446 
j Garrod's test for alkaptonuria, 247 
Gases in feces, 364 
in stomach, 349 
in urine. 254 
Gastric carcinoma, acetonuria in, 242 
contents, 308 

acetic acid in. 343 

acetone in, 348 

acidity of, 321-324. See also Hydrochlo- 
ric acid. 

Bacillus subtilis in, 350 

bacteria in, 350 

bile in, 351, 354 

blood in, 354 

Boas-Oppler bacillus in, 350 

butyric acid in, 342 

chemistry, 320 

chymosin in, 338 

composition, 308, 320, 350 

Congo-red test-paper for acidity, 322 

degree of acidity of, 323 

Einhorn's instrument for removing, 314 

fatty acids in, 342 

ferments in, 335 

free acids in, 321 

hydrochloric acid in, 321 

hyperacidity of, 324 

hypoacidity of, 324 

lactic acid in, 344. See also Lactic acid 
in stomach. 

Leptothrix buccalis in, 350 

microscopic study of, 350 

mucus in, 353 

organic acids in, 343 

parasites in, 355 

pepsin in, 335. See also Pepsin. 

products of digestion in, 340 

pus in, 355 

saccharomyces in, 350 

saliva in, 353 

Sarcinae ventriculi in, 350 

stomach-tube in collecting, 308. See also 
Stomach-tiibe. 

tissue shreds in, 351 



INDEX. 



549 



Gastric contents, total acidity of, 323 
zymogens in, 335 
digestion of albuminoids, 341 
of carbohydrates, 341 
of collagen, 341 
of elastin, 341 
of fat, 342 
of proteids, 340 
of starches, 341 
products of, 340 
hemorrhage, pulmonary hemorrhage and, 

differentiation, 448 
juice, alkaline, 324 
amount, 317 
blood in, 354 
characteristics of, 317 
chemic analysis of, 315 
examination, 315, 319 
excess of, 317 

hydrochloric acid in, 324. See also Hy- 
drochloric acid in gastric contents. 
odor, 352 

pepsin in, 335. See also Pepsin. 
stimulating flow of, 315. See also Test- 
meal. 
test-meal to stimulate, 315. See also 
Test-meal. 
Gastrosuccorrhea, 317 
Gayle, 511 

Genital organs, secretions of, 477 
Genito-urinary tract, actinomycosis of, 301 
Gentian, leukocytosis from, 103 
Gerhardt's test for diacetic acid, 243 
Gestation, vaginal secretion in, 483 
Glanders bacillus, diseases found in, 516 
in urine, 306 
bacteriuria in, 306 
blood in, 139 
nasal secretions in, 466 
pus of, 497 

Widal reaction in, 125 
Globin, Bence-Jones' albumose and, 220 
Globulicidal properties of blood-serum, 70 
Globulin in urine, 206, 214 

albumin and, separation, 206 
serum-, in blood, 64 
Glucose, glycuronic acid and, differentiating 
test, 229 
in blood, 67 

in urine, 224. See also Glucosuria. 
lactose and, differentiating test, 229 
Glucosuria, 224 
after glycerin, 225 
alimentary, 225 

differential density, test for, 235 
digestive, 226 
functional, 226 

glycuronic acid and, differentiation, 229 
intermittent, of arthritis, 226 
lactosuria and, differentiating test, 229 
nervous, 226 
puerperal, 225 
Roque's classification, 226 
saccharimeter for, 230, 236 
tests for, 226 
toxic, 225 
transitory, 225 
Glycerin, glucosuria after, 225 

ill urine, Cammidge's test, 531 
Glyc-ocliolic acid in feces, 368 
Glycogen in blood, 65 

in sputum, 451 
Glycuronic acid, glucose and, differentiating 
test, 229 
in urine, 239 
Goblet cells in feces, 375 
Goiiococci, Gram's stain for, 495 
ill urine, 303, 497 
methylene-blue for, 495 
Gonococci, staining, 494 
Gonorrhea, 494 



Gonorrhea, bacteriuria in, 303 
blood in, 139 
staining, 494 
staphylococci in, 496 
streptococci in, 496 
urethral, 483 - 
vaginal, 483 

Gonorrheal endocarditis, bacteria in blood 
in, 114 
gonococci in blood in, 114 

Gooch filter, 186 

Gram's method for gonococci, 495 

Granular basophiies, 91 
casts in urine, 284, 286 

Grape-sugar in urine, 224. See also Gluco- 
suria. 

Grass bacillus, tubercle bacillus and, differ- 
entiation, 441 

Gravimetric estimation of albumin in urine, 
213 

Greiss' test for nitrites in saliva, 454 

Guaiacum test for blood, 31 
for hemoglobinuria, 222 

Guanin in urine, 200 

Guinea-worm, 149 

Gum in urine, 239 

Gunning's mixture, 195 

Giinzburg's method for examining gastric 
juice, 319 

H^MAMCEBA, 154 

Haemogregarina, 155 

Haldane-Smith method for estimating vol- 
ume of blood, 31 
Halteridium, 155, 156 

Danilewskyi, 154 
Hammerschlag's method for estimating pep- 
sin, 337 
for specific gravity of blood, 40 
Hand centrifuge, 38, 39 
Hayem's solution, 52 
Hay-fever, nasal secretion in, 465 
Heart disease, organic, sputum in, 449 
Heart-disease cells, 449 
Hehner-Seemann's estimation of organic 

acids in stomach, 343 
Heller's test for hematuria, 221 
Helminthides, eosinophilia from, 106 
Helophilus, 410 
Hematin, 43 

in urine, 223 

spectrum of, 45 
Hematocrit, 38 
Hematocritization, 39 
Hematoidin, 43 

casts in urine, 2S5 

crystals in feces, 375, 379 
in urine, 270 
Hematoporphyrin, alkaline, 223 
Hematoporphyrinuria, 223 
Hematoxylin and eosin, 76, 77 
Hematozoon of Laveran, 153, See also J/g- 

larial parasite. 
Hematuria, 170, 221, 281 

malarial, 281 

tropic, 281 
Hemi-albumose, leukocytosis from, 104 
Hemoalkalimeter, Dare's, bi 
Hemochromogen, 41 
Hemocytolysis, 42, 141 
Hemocytometer, blood for, 52 

Oliver's, 58 

Thoma-Zeiss, 52 
Hemogelometer, 523 
Hemoglobin, 41 

carbonic-oxid, 43 
specti um of, 45 
tests for, 45 

in bk)Oii, (14 

ill pernicious anemia, 126 



55^^ 



INDEX. 



Hemoglobin in red cells, 41 
in urine, 222 
scale, Tallquist's, 51 
Wetherill's, 524 
Hemoglobinemia, 42, 137 
Hemoglobinometer, Dare's, 46 
Oliver's, 47, 48 
von Fleischl's, 48-51 
Hemoglobinuria, 222 
Hemokonia, 100 
Hemolysin, 117 
Hemophilia, blood in, 142 
Hemoptysis, endemic, 435 
Hemorrhage from bowels, color of stools 
after, 360 
pulmonary and gastric, difEerentiation, 
448 
Hemorrhagic exudates, 493 

eosinophilia from, 106 
Hemosiderin, 43 
Herpes tonsurans, 508 
Heteroxanlhin, 196 
in urine, 196, 200 
Hippuric acid in urine, 201 
Hippuric-acid crystals, 202 

in urine, 271 
Histon, Bence-Jones' albumose and, 220 

in urine, 223 
Hodgkin's disease, 132 
Honey-combed ring-worm, 506 
Hook-worm, 415 
disease, 386, 415 
in feces, 387, 415 
old-world, 416 
Hot baths and phosphates in urine, 182 
Human blood fluke, 146 

milk, 518. See also Milk. 
Humidity, quantity of urine and, 168 
Hyaline bodies, 159 

casts in urine, 284, 285 
Hydatid cyst, fluid of, 491 
parasite of, 404 
in sputum, 437 
Hydremia, blood in, 83 

in chlorosis, 128 
Hydrobilirubin in feces, 369 
Hydrochinon in urine, 256 
Hydrochloric acid, combined, in gastric con- 
tents, 333 
glucosuria after, 225 
in gastric contents, 321 
chymosin and, 338 
Cipollino's test, 533 
combined, 332, 333 
Congo-red test for, 330 
dimethylamido-azobenzol for, 328 
germicidal power, 327 
Mohr's test for, 331 
pepsin and, 335 

phloroglucin-vanillin test for, 329 
resorcin test for, 329 
test-papers for, 329 
tests for, 328 
tropaeolin test for, 331 
Hydrogen in feces, 364 
in stomach, 349 
sulphureted, in stomach, 349 
in urine, 254 
Hydronephrosis, fluid of, 490 
Hydroquinon, brown urine from, 171 

in urine, 256 
Hydrothionuria, 254 
Hydroxybutyric acid in urine, 240 
Hymenolepis diminuta, 407 

nana, 406 
Hyperacidity of gastric contents, 324 
Hyperchlorhydria, 326 
Hyperisotonic fluids, 73 
Hyperviscosity of blood, 88 
Hypisotonic fluids, 73 
Hypoacidity, 324 



Hypobromite method for estimating urea in 
urine, 193 
solution, 193 
Hypochlorhydria, 326 
Hypoderma bovis in keratitis, 472 
! Hj'podermoclysis, 73 
Hypoeosinophilia, 107 
Hypoleukocytosis, 104 
Hypoviscosity of blood, 89 
Hypoxanthin in urine, 200 



Icteric blood, 69 

Illumining microscope, 18 

Impetigo contagiosa, 514 

Inches, centimeter equivalents for, 526 

Incipient phthisis, sputum in, 447 

Indican in urine, 538 

Boston's test for, 211 
Indigo in urine, 277 
Indol in feces, 365, 366 

in sputum, 451 
Infectious diseases, acute. 133 
Inflammation of external auditory canal, para- 
sitic discharge from, 469 
Influenza bacillus in sputum, 443 

blood in, 138 
Infusoria in urine, 300 
Inhibition, Widal reaction and, 123 
Inoculation, animal, with blood, no 

of tubes, 463 
Inorganic sediments in urine, 260 

substances in blood, 65 
Inoscopy, 492 
Inosite in urine, 239 
Intestinal calculi in feces, 376, 377 
coccidiosis, 388 
concretions in feces, 376, 377 
parasites, 383 

Amoeba coli, 388 

Balantidium coli, 395 

blotting-paper test, 387 

cercomonas, 392 
hominis, 394 
intestinalis, 394 

cestodes, 396. See also Tape-worms. 

classification, 383 

coccidia, 388 

diagnosis, 386 

ectozoa, classification, 386 

entozoa, classification, 384 

examination of feces for, 386 

flagellata, 392 

flukes, 411 

helophilus, 410 

Lamblia duodenalis, 394 

macroscopic examination of feces for, 386 

magnifier for study of, 386 

mastigophora, 392 

Megastoma entericum, 394 

microscopic study of feces for, 387 

Paramcecium coli, 395 

protozoa, classification, 383 

questionable species, 409 

rhizopoda, 388 

round-worms, 414 

tape-worms, 396. See also Tape-worms. 

tetramitina, 392 

trematodes, 411 

trichomonas, 393 
sand, 377 
lodid of potassium, glucosuria after, 225 

in urine, 256 
lodin in urine, 255 

test for bile in urine, 240 
Ipecac, color of stools after, 361 
Iris diaphragm, 17 

in study of urine, 258 
Iron, color of stools and, 361 



INDEX. 



551 



Iron in sputum, 450 
Isotonic salts, 73 

tension in cholemia, 69 
of blood, toxins and, 108 
Itch, barber's, 509 

dhobie, 510 



Japanesk strongyle, 421 

Jaundice, blood in, 169 

Ja\vorski test for absence of pepsin, 337 

Jaworski-Karczyiiski test for blood in feces, 

360 
Jenner's stains for blood, 77, 78 



Karczyxski-Jaworski test for blood in feces, 

360 
Keg crystals, 265 
KelHng's test for lactic acid, 346 
Keratitis, discharge of, 471 

Hypoderma bovis in, 472 
Keratoconjunctivitis, 473 
Keratomycosis, 473 
Keratosis of pharynx, 460 
Kidney, cyst of, fluid of, 490 
Kjeldahl's method for nitrogen in urine, 195 
Klebs-Loffler bacillus in sputum, 442 

in urine, 306 
Klunge's test for blood, 355 
Koch flask, 109 
Koch-Weeks' bacillus, 475 
Kreatin in urine, 204 
Kreatinin, electric conductivity of, 175 

in urine, 204 
Kreatinin-zinc chlorid, crystals of, 205 



Lacmoid paper, preparation, 61 
Lactic acid in stomach, 344 
Boas' test for, 346 
KelHng's test for, 346 
tests for, 345 
Uf^elmann's test for, 345 
in urine, 244 
Lactodensimeter, Quevenne's, 520 
Lactoscope, Feser's, 521 
Lactose, glucose and, test to determine, 229 

in urine, 238 
Lactosuria,238 
glucosuria and, differentiating test, 229 
puerperal, 226 
Laiose in urine, 239 
Lamblia duodenalis in feces, 394 
Lancet, blood-, Daland's, 34 

fluke, 412 
Larvee in auditory canal, 470 
Laveran hematozoon, 153 
Lead, glucosuria after, 225 

in urine, 256 
Lead-workers, leukocytosis of, loi 

blood, basic degeneration of, 91, plate 4 
Leischman-Donovan bodies, 525 
Lenses, cleansing, 25, 26 
Leprosy bacillus, diseases found in, 516 
in blood, 140 
in pus, 497 

Bacillus tuberculosis and, 441 
bacteria in blood, 112 
blood in, 140 
exudate, 497 
nasal secretion in, 467 
Leptothrix buccalis in gastric fluid, 350 
in keratosis, 461 
in tartar, 459 
Leube's method to determine motor power of 

stomach, 318 
Leucin crystals in urine, 267, 269 
Leukemia, 129 
bacteria in blood in, 115 



Leukemia, lymphatic, 104, 129, 130, 131 
blood in, 132 

mixed, 129 

myeloid, 129, 130 

Charcot-Leyden crystals in blood in, 131 
Leukocytes, basophilic, 96 

counting, 52, 57 
method, 98,99 

decrease in, 104 

degenerated, 98 

effect of Hayem's solution on, 52 
of Toisson's solution on, 52 

eosinophilic, 94, 96 

in Amoeba coli, 392 

increase in, loi. See also Leukocytosis. 

in cyanosis, 84 

in diabetes, 69 

in disease, 96 

in myeloid leukemia, 130 

in sputum, 433 
color and, 430 

in urinary sediment, 278 
features, 282 

normal, 94 

number of, 94 

pipet for counting, 52 

polymorphonuclear, 94, 96 
neutrophils, 96 

polynuclear, 96 
basophils, 96 

transitional, 96 
Leukocytic shadows in diphtheria, 135 
Leukocytosis, 96, loi 

in abscess, 137 

in cystitis, purulent, 137 

in diphtheria, 135 

in erysipelas, loi, 138 

in osteomyelitis, 137 

in pernicious anemia, 127 

in plague, 139 

in pneumonia, 133 

in pyemia, 137 

in rheumatism, 138 

in scarlet fever, 135 

in septicemia, 137 

in serous effusions, 138 

in suppuration, 137 

in tonsillitis, 138 

in typhoid fever, 133 

in whooping-cough, 138 

of anesthesia, 102 

of malignancy, 102 

pathologic, loi 

physiologic, loi 

toxic, 102 
Leukopenia, 96, 104 

in influenza, 139 

in pernicious anemia, 127 
Levulose in urine, 239 
Light in microscopy, t8 

in study of urine, 258 
Lime in sputum, 450 
Lipaciduria, 250 
Lipemia, 66 
Lipuria, 251 
Liver fluke, 411 
Egyptian, 412 
narrow, 412 
Lochia, 485 
Lochia rubra, 4S5 

Locomotor ataxia, acetonuria in, 242 
Loffler bacillus in urine, 306 
Lowy 's method of estimating alkalinity of 

blood, 61 
Ludvvig's magnesia mixture, s2q 
Ludwig-Salkowski's estimation of uric acid, 

198 
Lumbar puncture, 500 
Lung, edema of, sputum in, 44S 

parasites of, animal, 435 



552 



INDEX. 



Lj-mphatic leukemia, 104, 129, 130, 131 
Lymphocytes, 94, 95 

in myeloid leukemia, 131 
Lymphocytosis, 104 

absolute, 105 

false, 105 
Lymphoid leukemia, 104, 129, 130, 131 
Lymphosarcoma, eosinophilia from, 106 



Macrocyte, 90 
Madura foot, 512 

Magnesia mixture, Ludwig's, 523 
Magnesium fluid, 183 
mixture, ammoniacal, 199 
phosphate in urine, 182 

basic, in urine, 271 
soap in urine, 266 
Magnifier for study of feces for parasites, 386 
Mai de Caderas, 151 
Mai de Coit, 151 
Malaria, 153 
crescentic bodies of, 162 
extracellular pigmented bodies of,'i62 
hyaline bodies in, 159 
oval bodies of, 162 
parasite of, 153, 157 
pigmented bodies in, 159 

extracellular, 162 
segmenting process of, 160 
sporules of, 161 
Malarial hematuria, 281 
parasite, 153, 157 
asexual cycle of, 167 
carbolthionin for, 158 
eosin and methylene-blue for, 158 
estivo-autumnai, staining, 158 
flagella of, 162-167 
human cycle of, 167 
life cycle of, 166, 167 
methylene-blue and eosin for, 158 
mosquito cycle of, 167 
passive flagellated. 165 
Plehn's method for, 158 
reproduction of, 166 
sporulation of, 161 
staining, 158 

Wright's method for, 158 
zoologic affinities of, 153 
Malignant disease, leukocytosis in, '102 

tumors, eosinophilia in, 106 
Mallory's bodies, 536 
Malnutrition, acetonuria in, 242 
Malta fever, blood in, 139 
Widal reaction in, 125 
Maltose in urine, 239 

test for, 341 
Mammary secretion, 517. See also Milk. 
Manganese dioxid, color of stools and, 361 
Marriage, sterile, 480 
Marrow, bone, bacteria in, 115, 116 
Marshall and Ryan's test for glucosuria, 233 
Mask for collecting spray, 427 
Mast cells, q6 
Mastigophora in feces, 392 
Mastzellen in myeloid leukemia, 131 
McNaught's modification of Cahn-Mehring 

estimation of fatty acids, 343 
Measles, acetonuria in, 242 

blood in, 136 
Measures, table of, 526 
Measuring of specimens, 26 
Megaloblasts, 92 
Megalocyte, 90 
Megalosporon ectothrix, 509 

endothrix, 509 
Megastoma entericum, 394 
Mehring-Cahn method for estimating fatty 
acids, McNaught's modification, 343 



Melancholia, acetonuria in, 242 
Melanemia, 94 
Melanin, 43 

Meningitis, epidemic, bacteria in blood in, 114 
diplococcus of, 502 

nasal secretion in, 466 
Menstrual fluid, 485 

after abortion. 485 
Mercury, glucosuria after, 225 

in urine, 256 

leukocytosis from, 104 
Metalbumin test for ovarian cyst, 491 
Metals in urine, 256 
Methane in feces, 364 
Methemoglobin, 42 

in urine, 223 

spectrum of. 45 
Methemoglobinuria, 223 

Methvlene-blue and eosin for malarial para- 
site, 158 

for gonococci, 495 

green urine from, 170 

solution, Gabbett's, 439 
Metric and English systems, relations, 526 
Microblast, 94 
Micrococci in pus, 498 
Micrococcus caprinus, 140 

melitensis, Widal reaction and, 125 
Microcyte, 90 
Micrometer, eye-piece, 27 

ocular, 27 

stage, 27, 28 
Micrometry, 26 
Microscope, 17 

adjustment wheel of, 24 

care of, 25 

condenser of, 25 

diaphragm of, 17 

iris, 17 » 

focus of, 22 

illuminating, 18 

lenses of, cleansing, 25, 26 

light for, 18 

micrometers for, 27, 28 

mirror in lighting, 19 
Microscopic cement, surrounding cover-glass 

with, 28 
Microsporon audouini, 507 

furfur. 510, 511 

minutissimum, 510, 511 
Middle-ear discharge, 468 
Miliarv tuberculosis, acetonuria in, 252 
Milk, 517 

Bacillus tuberculosis in, 519 

bacteria in, 519 

casein of, 518 

colostrum and, chemic differences, 517 

cow and human, 518 

fat in, 521 

human and cow, 518 

pathologic, 519 

proteids in, 522 

Staphylococcus epidermidis albus in, 519 
pyogenes aureus in, 519 

tube. 521 

tubercle bacillus in, 519 
Milk-curdling ferment, 338 
Milky urine, 252 
Millon's reagent, 217 

test for albumose, 217 
Mineral ash in urine, 178 
Mirror in lighting microscope, 19 
Mitosis of red cells iw leukemia, 130 
Moeller's grass bacillus, tubercle bacillus 

and, differentiation, 441 
Mohr's test for free hydrochloric acid, 331 
Molds in nasal secretion, 467 

in saliva, 454 

in sputum, 437 
Monomethylxanthin, 196 



INDEX. 



553 



Mononuclears, large, 95 
Monostomulum lentis,473 
Morax-Axenfeld diplobacillus, 475 
Morphin, alkaline phosphates in urine and, 
1S2 

glucosuria after, 225 

in urine, 257 

sulphates in urine and, 185 
Mountain spotted fever, parasite of, 155 
Mounting slide specimens, 80 
Mucin in saliva, 453 

in sputum, 451 

in urine, 205, 215, 249 
Boston's test for, 210 
differentiation, 215 
Ott's test for, 215 
Mucopurulent sputum, 431 
Mucor corymbifer in sputum, 438 
Mucous sputum, 431 
Mucus in vomit, 353 

Mullerand Weber test for blood in vomit, 354 
Mumps, cytodiagnosis of, 534 
Murexid test for uric acid, 196 
Musca vomitoria in feces, 411 
Mycetoma, 512 
Mycosis, discharge in, 456 

of external auditory canal, discharge, 469 

pharyngea leptothricia, 460 
Mycotic dermatitis, 510 
Myelocytes 97 

eosinophilic, 97 

in myeloid leukemia, 131 
Myeloid leukemia, 129, 130. See also Leuke- 

mia, myeloid. 
Myiasis, 513 
Myringomycosis aspergillina, discharge of, 

469 
Myxedema, blood in, 142 

Nagana, 151 

Naphthalin, brown urine from, 170 

in urine, 256 
Narrow liver fluke, 412 
Nasal secretion, 465-467 

ascarides in, 467 

Bacillus mallei in, 466 
of Friedlander in, 467 

cerebrospinal fluid in, 466 

Charcot-Leyden crystals in, 467 

Diplococcus intracellularis of Weichsel- 
baum in, 466 

entozoa in, 467 

Friedlander's bacillus in, 467 

fungi in, 467 

in bubonic plague, 467 

in glanders, 466 

in hay-fever, 465 

in leprosy, 4.67 

in meningitis, 466 

in ozena, 466 

in plague, 467 

in pneumonia, 467 

in tuberculosis, 466 

in typhoid fever, 467 

macroscopic appearance, 465 

molds in, 467 

oxyurides in, 467 

pathologic, 465 

pneumococcus in, 467 
_^reaction, 465 

rhodan in, 465 

Weichselbaum's Diplococcus intracellu- 
laris in, 466 
Necrosis of red cells, 92 
Needle-holder, Rosenberger's, 463 
Nephritis, acute, bacteriuria in, 304 

cocci in urine in, 304 
Nervous diseases, acetonuria in, 242 
Nessler's solution, 346 
Nest of beakers, 184 



Neutrophiles, 94 

polymorphonuclear, 96 

transitional, 98 
Newton's rings, 56 
Nitrate of urea, crystals of, 192 
Nitric acid, leukocytosis from, 104 
Nitric-acid test for biliary urine, 239 
Nitrite of amyl, glucosuria after, 225 
Nitrites in saliva, 454 
Nitrobenzol, glucosuria after, 225 
Nitrogen in feces, 364 

in urine, 254 
total, estimation, 195 

secretion, 192 
Nitromagnesium mixture, 207 
Noma of vulva, 484 
Normal blood, microscopic examination, 77 

salt solution, 73 
Normoblast, 93 

Nucleated red cells in pernicious anemia, 
127 
per cubic millimeter, 99 
Nucleic acid, leukocytosis from, 104 
Nuclein, eosinophilia from, 107 

in sputum, 451 

leukocytosis from, 104 

uric acid and, 196 
Nucleo-albumin. See Mucin. 
Nummular sputum, 431 
Nylander's test for glucosuria, 229 



Objective, cleansing, 26 
Oblique light in microscopy, 18 
Ocular, cleansing, 25 

micrometer, 27 
Oil, castor, leukocytosis from, 104 

croton, leukocytosis from, 104 

of anise-seed, leukocytosis from, 103 

of peppermint, leukocytosis from, 103 
Oil-immersion objective, focusing, 23 
Olein in blood, 66 
Oligemia, 94 
Oliguria, 169 
Oliver's hemocytometer, 58 

hemoglobinometer, 47, 48 

test for bile acid in urine, 240 
Onychomycosis, 511 
Opisthorcis sinense, 413 
Opium, leukocytosis from, 104 

poisoning, saliva in, 453 
Optical saccharimeter, 236 
Organic acids, Congo-red test and, 331 
in gastric contents, 343 

heart-disease, sputum in, 449 

sediment in urine, 278 
Organized casts in urine, 2S4 
Osmosis, cryoscopy and, 72 

of blood, 73 
Osmotic tension, 73 
Osteomyelitis, blood in, 137 
Otitis media, discharge in, 468 
Otomycosis, discharge of, 469 
Ott's test for mucin, 215 

for nucleo-albumin, 215 
Oval bodies in malaria, 162 
Ovarian cysts, 490 

metalbumin test for, 4qi 
Oxalate of calcium, amorphous, in urine, 274 

in urine, 265 

of urea, crj'stals of, 192 
Oxalic acid in urine, 203 
Oxalic-acid diathesis, 203 
Oxaluria, 203, 265 
Oxybutyric acid iiv urino, 2p 
Oxygen in urine, 254 
Oxyhemoglobin, 42 

spectrum of, 44 
Oxyurides in nasal secretion, 467 

in vaginal secretion, 4S4 



554 



INDEX. 



Oxyuris vermicularis, 414 

in blood, 143 

in urine, 297 
Ozena, bacillus of, 467 

nasal secretion in, 466 
Ozonic ether, 222 



Palmitin in blood, 66 
Pancreatic cyst, fluid of, 491 
Pancreatin, glucosuria after, 225 
Paragonimus Westermanii in sputum, 435 
Paralysis of insatie, acetonuria in, 242 
Paramido-acetophenone solution, 243 
Paramoecium coli, 395 

Parasites, animal, in feces, 383. See also 
Intestinal parasites. 
in pus, 497 
in urine, 292 

Stiles' key to, 299 
in vaginal secretions, 484 
of lung, 435 
in vomit, 355 
intestinal, 383 

of smallpox, vaccinia and varicella, 536 
vegetable, in urine, 300 
Parasitic cysts of eyelids, 476 
diseases of blood, 143 
hemoptysis, 435 
Paratyphoid fever, Widal reaction and, 124 
Paraxanthin in urine, 200 
Paresis of insane, acetonuria in, 242 
Parkes' classification of urinary constitu- 
ents, 177 
Passive flagellated parasite, 165 
Paton's test for globulin, 214 
Pentoses in urine, 238 
Pentosuria, 238 

Peppermint oil, leukocytosis from, 103 
Pepsin, 335 
absence of, 337 
destruction of, 335 
Hammerschlag's method for estimating, 

337 
hydrochloric acid and, 335 
Jaworski's test for absence of, 337 
leukocytosis from, 104 
tests for, 336 
zymogen of, 335 
Pepsinogen, 335 
Peptone in blood, 64 
in sputum, 451 
in urine, 217 
biuret reaction with, 217 
Boston's test for, 210 
Salkovvski's test for, 217 
leukocytosis from, 104 
source of, 341 
Pernicious anemia, 126 

color-index of blood in, 126 
differential diagnosis, 128 
hemoglobin in, 126 
leukocytosis in, 127 
leukopenia in, 127 
nucleated red cells in, 127 
oxygen of blood in, 126 
poikilocytosis in, 127 
red corpuscles in, 126 
teeth in, 459 
Pertussis, blood in, 138 
Petri dish for fixing blood spreads, 74 
Pettenkofer's test for biliary acids in blood 
serum, 69 
in feces, 369 
Pharyngomycosis leptothricia, 460 
Pharynx, keratosis of, 460 
Phenol in feces, 365, 366 

in sputum, 451 
Phenylhydrazin test for alkaptonuria, 247 
for glucosuria, 229 



Phlegmon, 493 

Phloridzin, glucosuria after, 225 

Phloroglucin test for pentosuria, ToUen's, 

239 
Phloroglucin-vanillin test for free hydro- 
chloric acid, 329 
Phosphate, ammoniomagnesium, in urine, 
271 

in feces, 379 

in urine, 181, 267 
alkaline, 181, 182. See also Urine, phos- 
phates in, alkaline. 
earthy, 181, 182. See also Urine, phos- 
phates in, earthy. 

of calcium in feces, 379 
in urine, 267 

of magnesium, basic, in urine, 271 

triple, in alkaline urine, 275 
in feces, 379 
in urine, 271 
Phosphatic earths, basic, in urine, 277 
Phosphoric acid, alkaline phosphates in urine 
and, 183 
in urine, 181 
Phosphorus, eosinophilia from, 107 

glucosuria after, 225 

poisoning, polycythemia from, 88 
Phthisis, acetonuria in, 242 
Picric-acid test for glucosuria, 229 
Pigment, blood, spectroscopic examination. 

for, 43 
Pigmented bodies, extracellular, 162 
in estivo-autumnal fever, 160 
in malaria, 159 
in quartan fever, 160 
in tertian fever, 160 
Pigments, urinary, Boston's test for, 210 
Pile crystal, 275 
Pilocarpin, eosinophilia from, 107 

leukocytosis from, 104 
Pinta, 512 

Pipet for counting corpuscles, 52 
Piroplasma, 155 

Pirosoma bigeminum, 154, 155, 157 
Pityriasis versicolor, 511 
Pjudi, 151 
Plague, bacteria in blood in, 114 

blood in, 139 

nasal secretion in, 467 

Widal reaction in, 124 
Plasma, estimation, 38 

osmotic properties, 273 
Plasmodium malariae, 157. See also Mala- 
rial parasite. 
Plehn's method for malarial parasites, 158 
Pneumococcus, capsule of, stain for, 444 

in nasal secretion, 467 

in sputum, 444, 449 

Widal reaction and, 125 
Pneumoconiosis, sputum in, 449 
Pneumomycosis, Aspergillus fumigatus and, 

437 
Pneumonia, acetonuria in, 242 

bacteria in blood in, 153 

blood in, 133 

nasal secretion in, 467 

sputum in, 448 

Widal reaction in, 125 
Podophyllin, leukocytosis from, 104 
Poikilocyte, 90 
Poikilocytosis in pernicious anemia, 127 

in secondary anemia, 89 
Poisons in stomach, tube for removal, 314 

in urine, 256 

polycythemia from, 88 
Polariscope for sugar in urine, 230, 236 
Polarizing saccharimeter, 236 
Polychromatophilia, 91, 93 
Polycythemia, 84 

from anesthesia, 85 



INDEX. 



555 



Polycythemia from carbonic oxid, 88 

from phosphorus, 88 

from vasoconstriction, 84, 108 

in leprosy, 140 

local. 84 

of poisons, 88 
Polyglobulia, 524 

Polymorphonuclear neutrophiles, 96 
Polynuclear basophils, 96 

leukocytes, 96 
Polyuria, 169 
Pork tape-worm, 398 

in blood, 147 
Potash, caustic, leukocytosis from, 104 
Potassic cupric tartrate, solution of, 227 
Potassium bromid, alkaline phosphates in 
urine and, 182 
sulphates in urine and, 185 

in urine, 177 

iodid, glucosuria after, 225 
in urine, 256 

salts in saliva, 453 

urate, acid amorphous, in urine, 275 
Propepsin, 335 
Propionic acid in feces, 368 

in urine, 250 
Proteids, digestion of, 340 

in milk, estimation, 522 

in sputum, 451 

in urine, 205 
Proteosoma, 155 

relicta, 154 
Prothrombi, 64 
Protozoa, classification, 3S3 

in exudates, 536 

in pus, 497 «\«^ 
Protozoic dermatitis, 512 
Pruritus vulvce, discharge in, 486 
Pseudoleukemia, 132 
Pseudopods, 388, 390 
Ptomains in urine, 254 
Ptyalin, carbohydrate digestion and, 341 
Puerperal glucosuria, 225 

lactt)suria, 226 
Pulmonary abscess, sputum in, 445 

gangrene, sputum in, 446 

hemorrhage, gastric hemorrhage and, dif- 
ferentiation, 448 

tuberculosis, sputum in, 447 
Punctate basic degeneration of red cells, 91 
Puncture, lumbar, 500 
Purdy's tubes for centrifuge, 189 
Purgation, leukocytosis from, 104 
Purin bases, 196, 200 

exogenous, 523 
in feces, 553 

in urine, estimation, 529 
Purinometer, 529 
Purinometer, 523 
Purpura, bacteria in blood in, 114 

haemorrhagica, blood in, 141 
Purulent cystitis, blood in, 137 

exudates, 493. See also Pus. 
Pus, 493 

animal parasites in, 497 

casts in urine, 288 

fungi in, 498 

in feces, 376 

in urinary sediments, 278 
leatures, 282 

in urine, 246 
differentiation, 215 

in vomit, 355 

organisms of, in blood, 114 

parasites in, animal, 497 

protozoa in, 497 

urethral, 494. See also Gouoi rhca. 
Pus-producing organisms in feces, 3S1 
Putrescin in urine, 254 
Putrid bronchitis, sputum in, 446 



Pyelitis, bacteriuria in, 307 
Pyemia, bacteriuria in, 304 

blood in, 137 

cocci in urine, 304 
Pyknometer, 213 

Pyocyanin, leukocytosis from, 104 
Pyrocatechin, brown urine from, 171 
Pyuria, 246 

Quantitative anemia, 94 
Quartan fever, 159 

hyaline bodies in, 159 
parasite of, 160, 161 
pigmented bodies in, 159 
parasite, 160, 161 
Quevenne's lactodensimeter, 520 
Quinin, alkaline phosphates in urine and, 183 
color of urine and, 171 
in urine, 256 
leukocytosis from, 104 

Ravold's test for albumin, 526 
Ray fungus. See Actinotmces. 
Red bone-marrow, bacteria in, 115, 116 
corpuscles, 81 

altitudes and , 86 

ameboid movements of, 90 

Cabot's ring-bodies in, 91 

counting, 52, 56 

decoloration of, in anemia, 89 

effect of Hayem's solution on, 52 
of Toisson's mixture on, 52 

estimation of, 38 

granular basophilia in, 91 

hemoglobin in, 41 

in Amoeba coli, 392 

in anemia, 82 

in burns, 85 

in cholemia, 69 

in cyanosis, 84 

in diabetes, 68 

in feces, 375 

in hemocytolysis, 141 

in myeloid leukemia, 130 

in pernicious anemia, 126 

in polycythemia, 84 

in scarlet fever, 135 

in secondary anemia, 88 

in sputum, 433 

in urinary sediment, 2S1, 2S2 

mitosis of, in leukemia, 130 

motility of, in secondary anemia, 89 

necrosis of, 92 

nucleated, in chlorosis, 128 
in leprosy, 140 
in pernicious anemia, 127 
per cubic millimeter, 99 

number of, 81 

Oliver's hemocytometer for countirg, 58 

osmosis of, 73 

pipet for counting, 52 

polychromatophilia of, 91, 03 

punctate basic degeneration, 91 

shape of, in secondary anemia, 89 

size of, in secondary anemia, 89 

specific gravit\- of, increased, S3 

staining, at>pical, qo 

water in, S3 
Reduced hemoglobin, 42 

spectrum of, 4s 
Reflected light, iS^ 
Reinecke's test for pus in urine, 246 
Relapsing fever, bacteria in blood in, 111 

bacteriuria in, 306 
Renal casts, 2S3 

amvloid, 280 

blood, 284, 287 

composite, 284, 2S9 

composition, 283 

cylindroid, 2S4, 290 



S56 



INDEX. 



Renal casts, epithelial, 288 

false, 284, 290 

fatty-acid, 289 

granular, 284, 286 

hematoidin, 285 

hyaline, 284, 285 

mounting, 259 

organized, 284 

preservation, 259 

pus, 288 

staining, 284 

unorganized, 283 

urate, 284 

waxy, 289 
cysts, 490 
Resinous bodies in urine, Boston's test for, 

211 i 

Resorcin, brown urine from, 170 
in urine, 256 

test for free hydrochloric acid, 329 
Rhabditis genitalis in urine, 297 
Rhamnose in urine, 238 
Rheostat and electric centrifuge, 38 
Rheumatism, acute articular, acetonuria in, 
242 

blood in, 138 
Rhizopoda in feces, 388 
Rhodan in nasal secretion, 465 
Rhubarb, urine and, 171, 256 
Riegel's test-dinner, 316 
Rigler's test for glucosuria, 230 
Ringing of specimens, 28 

turntable for, 29 
Ring-worm, honey-combed, 506 
Robert's solution, 207 
Rocky-Mountain tick, 155 
Roque's classification of glucosuria, 226 
Rosenberger's needle-holder, 463 
Rouleaux formation in secondary anemia, 88 
Round-worms, 414 
Ruhemann's estimation of uric acid, 530 

uricometer, 530 
Rusty sputum, 430 
Ryan and Marshall's test for glucosuria, 233 



Saccharimeter, 236 

Einhorn's, 230 

for alkaptonuria, 247 

optical, 236 

polarizing, 236 

Ultzmann's, 236, 237 
Saccharomyces in gastric fluid, 350 
Salicylate of sodium, sulphates in urine and, 

185 
Salicylates in urine, 256 
Salicylic acid in urine, 256 
Saliva, 452 

actinomyces in, 458 

albumin in, 453 

bacillus fusiform in, 455, 456 

bacteriology of, 454 

corpuscles of, 454 

cultures from, 4.55, 461 

diastatic ferment in, 453 

epithelia in, 454 

ferment in, 453 

fungi in, 454. 457 

fusiform bacillus in, 455, 456 

in actinomycosis, 458 

in angina with ulcerative stomatitis, 455 

in disease, 455 

in opium poisoning, 453 

in stomatitis, catarrhal, 455 
gonorrheal, 457 
ulcerative, with angina, 455 

in thrush, 457 

in vomit, 353 

molds in, 454 

mucin in, 453 



Saliva, nitrites in, 454 

potassium salts in, 453 

reaction, 452 

spirillum of Vincent in, 455, 456 

sugar in, 453 

sulphocyanids in, 453 

Vincent's spirillum in. 455, 456 
Salkowski's estimation of xanthin bases, 
201 

modification of Volhard's method for 
chlorids in urine, 180 

test for peptone, 217 
Salkowski-Ludwig's estimation of uric acid, 

198 
Salol in urine, 256 
Salzer's test-meal, 311 
Sand, intestinal, 377 
Santonin, color of stools after, 361 

yellow urine from, 171 
Sarcinae in sputum, 437 

ventriculi in gastric fluid, 350 
Sarcolactic acid in urine, 244 
Sarcoma, eosinophilia from. 106 
Scammony, leukocytosis from, 104 
Scarlet fever, acetonuria in, 242 
bacteria in bone-marrow in, 116 
bacteriuria in, 306 
blood in, 135 
Mallory's bodies in, 492 
Schistocyte, 90 
Schistosoma bovis, 146 

haematobium, 146 
in pus, 497 
in sputum, 436 
in urine, 295 
Screw-worm, 513 
Scrum-pox, 510 
Scurvv, blood in, 142 
Sea-bathing, phosphates in urine and, 

183 
Secondary anemia, 82. 88 
Sedimentation of urine, 257 
Segmenting bodies of malaria, 160 

of quartan fever, 161 
Semen, 477 

bacteria in, 480 

Charcot-Leyden crystals in, 478 

chemistry, 478 

collection, 477 

microscopic study, 47S 

pathology, 480 
Senna, color of stools after, 361 

urine and, 171, 256 
Septicemia, acetonuria in, 242 

bacteriuria in, 304 

blood in, 137 

cocci in urine in, 304 
Seropurulent exudates, 492 
Serous effusions, blood in, 138 

exudates, 492 

sputum, 432 
Serum, blood-, 69, 70 
Serum-albumin in blood, 64 

in sputum, 4SI 

in urine. 206. See also Albumin in 
urine. 
Serum-diagnosis. 116 

Picker's for typhoid fever. 525 
Serum-globulin in blood, 64 

in urine, 206, 214 
Shadow cell, 89, 91 
Shiga bacillus, 381 
in feces, 381 

Widal reaction and, 124 
Siderosis, sputum in, 450 
Sievers-Ewald's method for motor power of 

stomach, 318 
Silicates in sputum, 450 
Silver in urine. 256 
Silver-carbonate test for uric acid, 197 



INDEX. 



557 



Simon'5 estimation of hippuric acid, 202 
Skatol in feces. 365, 366 

in sputum, 451 
Skin diseases, 506 
Sleeping sickness, 153 
Slides, 35 

blood-fixing, 74 

cleansing, 32 

labels for, 80 

mounted, ringing of, 28, 29 

mounting, 80 

preparation, 32 
Smallpox, blood in, 136 

parasite of, 536 
Small's stain for gonococci, 495 
Smears, blood, 35 
Smegma bacillus, Bacillus tuberculosis and, 

differentiation, 441 
Smith-Haldane method for estimating volume 

of blood, 31 
Soaps in urine, 266 
Soda bicarbonate, leukocytosis from, 104 

urate of, leukocytosis from, 104 
Sodium chlorid in urine, 179 

hydrate solution, normal, 323 

in urine, 177 

salicylate, sulphates in urine and, 185 

urate, acid, in urine, 273 
Specific gravity beads, 173, 174 
Specimens, measuring of, 26 

ringing of, 28 
turntable for, 29 
Spectra of blood, 43 

of carbonic-oxid hemoglobin, 45 

of hematin, 45 

of hemoglobin, carbonic-oxid, 45 
reduced, 45 

of methemoglobin, 45 

of oxyhemoglobin, 44 

of reduced hemoglobin, 45 
Spectroscope, Browning's, 43, 44 

in testing for blood, 45 
Spectroscopic study of blood, 41-43 
Spermatozoa, 478 

absence of, 480 

in urine, 291 

of mammals, 479 

preservation, 477 

stains for, 480 
Spheric bodies of malaria, 162 
Spinal fluid, cytologic study, 538 
Spirillum of Vincent in saliva, 455, 456 
Spleen extract, leukocytosis from, 104 

removal of, eosinophilia from, 106 
Splenic anemia, 132 
Sporulation of malarial parasite, 161 
Sporules of malaria, 161 
Spotted fever, mountain, parasite of, 155 
Spray, throat, collection of, 427 
Sputum, 426 

actinomyces in, 437 

albumin in, serum-, 451 

Amoeba coli in, 436 

anthracotic, 430 

ascarides in, 437 

Aspergillus fumigatus in, 437 
nigerin,437 

bacjllus of Friedlander in, 445 
tuberculosis in, 438 

bacteria in, 438 

Balantidium coli in, 436 

bilharzia in, 436 

black, 430 

blood in, in tuberculosis, 447, 448 

bloody, 430 

bronchial spirals in, 433 

caseous particles in, 431 

casts in, 433 

characteristics of, 428 

Charcot-Leyden crystals in _;33 
asthma, 445, 446 



Sputum, chemic study of, 450 
coal-dust in, 449 
collection, 426 
color, 430 
cup, 426 

Curschmann spirals in, 433 
diphtheria bacillus in, 442 
Distomum pulmonale in, 435 

ringeri in, 435 
elastic fibers in, 434 
epithelia in, 433 
fatty acids in, 451 
ferments in, 451 
fibrinous coagula in, 432 
Filaria sanguinis hominis in, 437 
Friedlander's bacillus in, 445 
fungi in, 437 
glycogen in, 451 
gray, 430 
green, 430 
in anthracosis, 44q 
in asthma, bronchial, 445 
in bronchial asthma, 445 
in bronchitis, 443, 444 

putrid, 446 
in bronchopneumonia, 445 
in chalicosis, 450 
in edema of lung, 448 
in endemic hemoptysis, 435 
in heart disease, organic, 449 
in organic heart disease, 449 
in pneumoconiosis, 449 
in pneumonia, 448 
in pulmonary abscess, 445 

gangrene, 446 

tuberculosis, 447 
in putrid bronchitis, 446 
in siderosis, 450 
in stycosis, 450 
indol in, 451 

influenza bacillus in, 443 
iron in, 450 

Klebs-Lofifler bacillus in, 442 
leukocytes in, 433 

color and, 430 
lime in, 450 

microscopic study of, 432, 438 
molds in, 437 
mucin in, 451 
mucopurulent, 431 
Mucor corymbifer in, 438 
mucous, 431 
nuclein in, 451 
nummular, 431 
odor, 429 

organic substances in, 450 
organized constituents of, 43i 
Paragonimus Westermanii in, 435 
peptones in, 451 
phenol in, 451 
pneumococcus in, 444, 449 
proteids in, 451 
reaction, 430 
red corpuscles in, 433 
rusty, 430 
sarcinae in, 437 

Schistosoma hiematobium in, 436 
serous, 432 

serum-albumin in, 451 
silicates in, 450 
skatol in, 451 
specific gravity, 430 
spirals in, bronchial, 433 

Curschmaim's, 433 
staphylococcus bronchitis in, 443 
streptococcus bronchitis in, 443 
Tienia echitiococcus 111,437 
tenacity, 4211 
trichomonas in, 430 



538 



INDEX. 



Sputum, tubercle bacillus in, 438. See also 
Bacillus tuberculosis. 
whooping-cough protozoon in, 436 
yeasts in, 437 
Squibb's urinometer, 175 
Stage micrometer, 27, 28 

Stains, anilin-gentian-violet, for tubercle 
bacillus, 440 
carbolthionin, for malarial parasite, 158 
Ehrlich's tricolor, 79 
eosin and hematoxylin, 76, 77 
and methylene-blue, for malarial parasite, 
158 
for Amoeba coli, 392 
for Bacillus tuberculosis, 438 
for bacteria in urine, 302 
for blood, 76, no 

Ehrlich's tricolor, 79 
eosin and hematoxylin as, 76 
fixing combined with, 77 
Jeimer's, 78 

combined with fixing, 77 
Wright's, 78, 79 
for casts, 284 

for cerebrospinal fluid, 502 
for cystic fluids, 489 
for estivo-autumnal parasite, 158 
for exudates, 489 
for fat in urine, 225 
for filaria, 148 
for gonococcus, 494 
for malarial parasite, 157 
for pneumococcus, 444 
for purulent exudates, 494 
for pus, 494 

for red corpuscles, atypical, 90 
for renal casts, 284 
for spermatozoa, 480 
for throat cultures, 463 
for transudates, 489 
for trypanosoma, 153 
for tubercle bacillus, 438 
for urinary sediments, 258 
Gram's, for gonococci, 495 
hematoxylin and eosin, 76, 77 
Jenner's, 78 

with fixing combined, 77 
methylene-blue and eosin, for malarial 
parasite, 158 
for gonococci, 495 
Plehn's, for malarial parasite, 158 
Small's, for gonococci, 495 
Sterling's, for tubercle bacilli, 440 
Wright's, for blood, 78, 79 
for malarial parasite, 15S 
Staphylococcus bronchitis in sputum, 443 
epidermidis albus in milk, 519 
haemorrhagicus, 511 
in feces, 381 
in gonorrhea, 496 
in pus, 498 
in tartar, 459 

pyogenes albus, diseases found in, 516 
in urine, 307 
aureus, diseases found in, 516 
in milk, 519 
in urine, 307 
citreus, diseases found in, 516 
Starch, gastric digestion of, 341 
in feces, 372 

in urinary sediment, 282 
in urine, 253 
solution, 347 
Stearin in blood, 66 
Stercobilin in feces, 369 
Stercoraceous vomit, 354 
Sterigmatocystis Candida in ear discharge, 

469 
Sterile marriage, 480 
Sterling's stain for tubercle bacillus, 440 



Sternberg's bacillus in urine, 306 

Stiles' key to parasites of urine and vagina, 

299 
Stomach, gases in, 349 

motor power of, 318 

poisons in, removal, 314 

resorptive power of, 319 

washing, 313 
Stomach-contents, 308. See also Gastric 

contetits. 
Stomach-tube, 308 

aspiration with, 313 

Boas' aspirator attachment, 309, 310,313 

counterindications, 309 

in collecting gastric contents, 308 

introduction, 309, 313 

removal, 314 
of poisons by, 314 

washing stomach through, 313 
Stomatitis, catarrhal, saliva in, 455 

gonorrheal, saliva in, 457 

ulcerative, with angina, saliva in, 455 
Stools, bilious, color of, 361 

clay-colored, 361 

in constipation, 357, 358 

in diarrhea, 351 

fatty, 378 

form, 359 

mucoid, 372 

serous, 372 
Streptococcuria, 304 
Streptococcus bronchitis in sputum, 443 

in feces, 381 

in gonorrhea, 496 

in pus, 498 

in tartar, 459 

in urethral pus, 496 

pyogenes, diseases found in, 516 
erysipelatis in urine, 306 

of Fehleisen, diseases found in, 516 
Streptocolysin, 117 
Streptocolysis, 117 
Strongyloides intestinalis, 419 

in blood, 143 

in feces, 422 

subtilis,42i 
Strvchnin, alkaline phosphates in urine and, 
'183 

glucosuria after, 225 

in urine, 256 
Stycosis, sputum in, 450 

Sulphate of calcium, amorphous, in urine, 
274 

crystals in urine, 266 
Sulphates in urine, 185. See also Urine, sul- 
phates in. 
Sulphid of bismuth in feces, 380 
Sulphocyanids in saliva, 453 

solution, standardizing, 180 
Sulphonal, color of urine and, 171 
Sulphur in urine, loosely combined, 187 

neutral, estimation, 187 

oxidized, estimation, 187 
Sulphureted hydrogen in stomach, 349 

in urine, 254 
Sulphuric acid, glucosuria after, 225 

in urine, 185 
Suppuration, bacteria in blood in, 113, ii.'", 

blood in, 137 
Surra, 151 
Synovial fluid, 504 



TAENIA Africana, 409 

cucumerina, 407 

echinococcus, 404 

in sputum, 437 

in urine, 292 

flavopunctata, 407 



INDEX. 



559 



Taenia lata cxf Linne, 402 

niadagascariensis, 409 

marginata, 400, 406 

mediocanellata, 399 
blood and, 147 

nana, 406 

saginata, 399 
in blood, 147 

solium, 39S 
in blood, 147 
Takosis, blood in, 140 
Tallquist's hemoglobin scale, 51 
Tape-worms, 396 

beef, 399 

detection of head, 397 

dog, 400, 406 
double-pored, 407 
small, 404 

dwarf, 406 

fish, 402 

head of, 396, 397 

in blood, 147 

in feces, 396 

pork, 398 
in blood, 147 

proglottides of, 396 

removal of, 396 

segments of, 396 
Tartar of teeth, 458 
Taurocholic acid in feces, 368 
Tear stone, 475 
Teeth in pernicious anemia, 459 

tartar of, 458 
Teichmann's test for blood, 31 
Temperature, quantity of urine and, 168 
Tertian fever, hyaline bodies in, 159 
parasite of, 160 
fiagella of, 162 
pigmented bodies in, 159 
extracellular, 162 
Test-meal, 315 

Boas' breakfast, 316 

Ewald-Boas' breakfast, 315 

Riegel's dinner, 316 

Salzer's, 316 
Tetanus exudate, 497 
Tetramitina in feces, 392 
Texas fever, parasite of, 154, 155, 157 
Thallin in urine, 256 
Theobrorain, 196 
Theophyllin, 196 
Thermometric equivalents, 526 
Thoma-Zeiss hemocytometer, 52 
Thorn-apple crystals, 272, 276 
Throat, cultures from, 461 

examination of, 462 

spray from, 427 
Thrush, saliva in, 457 
Thymus extract, leukocytosis from, 104 
Thyroid extract, glucosuria after, 225 

leukocytosis from, 103 
Tinea barbae, 509 

circinata, 509 
tropic, 509 

favosa, 506 

sycosis, 509 

tonsurans, 507 

trichophyton endothrix, 509 

tropic, 509 

versicolor, 510, 511 
Tissue shreds in gastric contents, 351 
Toisson's mixture, effect on leukocytes, 52 
on red cells, 52 
for blood for hemocytometer, 52 
Tollen's phloroglucin test for pentosuria, 

239 
Tongue, coating of, 458 
Tonsillar membrane, 459 

cultures from, 461 
Tonsillitis, acetonuria in, 242 



Tonsillitis, blood in, 138 

membrane in, 459 
Topfer's estimate of hydrochloric acid, 332 
Torfugation, 528 
Torkritization, 523 
Toxicity of blood-serum, 70 
Toxins, effect on tension of blood, 108 
Trachoma, 475 
Transitional leukocytes, 96 
light, 18 
neutrophiles, 98 
Transudates, 487 
Trematodes, 411 

of eye, 472 
Trichina spiralis in blood, 146 
Trichinella spiralis, 422 
Trichinosis, blood in, 146 

eosinophilia from, 106 
Trichocephalus dispar, 418 
in blood, 143 
in urine, 298 
hominis, 418 
Trichomonas in feces, 393 
in sputum, 436 
vaginalis, 484 
in urine, 300 
Trichophyton endothrix, 511 
microsporon, 507 
tonsurans, 508 
Triple phosphates in alkaline urine, 275 
in feces, 379 
in urine, 182, 271 
Tropaeolin test for hydrochloric acid, 331 
Tropic hematuria, 281 

tinea, 509 
Trypanosoma, 151 
gambiense, 151 
hominis, 151 
in pus, 498 

sleeping sickness and, 153 
Trypanosomiasis, 151 

spinal, filaria and, 148 
Tsetse-fly disease, 151 
Tube-casts, 283. See also Renal casts. 
Tubercle bacillus. See Bacillus tuberculo- 
sis. 
Tuberculin, glucosuria after, 225 

leukocytosis from, 104 
Tuberculosis, bacteria in blood in, 112 
in bone-marrow in, 116 
bacteriuria in, 303 
miliary, acetonuria in, 242 
milk in, 519 
nasal secretion in, 466 
of throat, detection, 464 
pulmonary, sputum in, 447 
Widal reaction in, 125 
Tumor fragments in urine, 291 

malignant, eosinophilia from, 106 
Tiirck's stimulating forms, 98 
Turntable for ringing specimens, 29 
Typhoid fever, acetonuria in, 242 
bacillemia with, 112 
bacteria in blood in, 112 
in bone-marrow in, 116 
bacteriuria in, 305 
blood in, 133 
diazo-reaclion for, 249 
Picker's reaction in, 525 
nasal secretion in, 467 
Widal reaction in, nS, 124 
Tyrosin crystals in urine, 267, 268 
in feces, 365 



Ufkelmann's test for lactic acid, 345 
Ulcerative endocarditis, bacteria in blood in 

, i'4 . . . 

bacteria ot, \\\ urnie, 304 



560 



INDEX. 



Ultzmann's estimation of earthy phosphates 
in urine, 183 
saccharimeter, 236, 237 
Uncinaria, 415 
americana, 416 

niegaloblasts in, 92 
duodenale, 416 
blood in, 143 
serum reaction in, 143 
Uncinariasis, 415 
Unorganized casts in urine, 283 
Uranium solution, 1S4 
Urate casts, 284 

Urates, acid-ammonium, in urine, 272 
amorphous, in urine, 274 
electric conductivity of, 175 
in urine, Boston's test for, 210 
of ammonium in alkaline urine, 276 
of calcium, acid amorphous, in urine, 275 
of soda, leukocytosis from, 104 
potassium, acid amorphous, in urine, 275 
sodium, acid, in urine, 273 
turbid urine and, 171 
Urea, 192 
electric conductivity of, 175 
in blood, 65 
in urine, 192 
chlorids and phosphates and, ratio, 193 
ureometer for, 194 
nitrate, crystals of, 192 
oxalate, crystals of, 192 
Urein in urine, 248 
Ureometer, Doremus, 194 

Hinds' modification, 194 
Urethral gonorrhea, 483 

pus, 494 
Urethritis, gonococci in, 496 
blood in, 139 
streptococci in, 406 
Uric acid, electric conductivity of, 175 
in blood, 65 
in urine, 196 
carbonate-of-silver test for, 197 
copper test for, 197 
Ludwig-Salkowski's estimation, 198 
murexid test for, 196 
quantitative estimation, 530 
Salko\vski-L\id\vig's estimation of, 198 
silver-carbonate test for, 197 
tests for, 196 
leukocytosis from, ro4 
Uric-acid crystals in urine, 264 
Uricometer, Ruhemann's, 530 
Urinary concretions in urine, 278 
pigments, Boston's test for, 210 
sediments, 257, 260 
alkahne, 275 

ammoniomagnesium phosphates, 271 
ammonium urates, acid, 272 

alkaline, 276 
amorphous, 274 

alkaline, 277 
bilirubin, 270 
blood in, 281 
boric acid, 267 
calcium carbonate, 277 
oxalate, 265 

amorphous, 274 
phosphates, 267 
soap in, 266 
sulphate, 266 

amorphous, 274 
urate, acid amorphous, 275 
carbonate of calcium, 277 
casts in, 283. See also Renal casts. 
cholesterin, 272 
concretions, urinary, 278 
cystin, 271 
dark bodies, 274 
epithelia in, 279, 282 



Urinary sediments, fat, 274 

focus for, 258 

hematoidin, 270 

hippuric acid, 271 

in acid urine, 260 

in alkaline urine, 260 

indigo, 277 

inorganic, 260 

leucin, 267, 269 

leukocytes in, 278, 282 

light in study of, 258 

magnesium phosphates in, basic, 271 
soap, 266 

microscopic technic, 258 

organic, 278 

oxalate of calcium, amorphous, 274 

permanent mounts for, 258 

phosphates of calcium, 267 
of magnesium, basic, 271 
triple, 271 
alkaline, 275 

phosphatic ammoniomagnesium, 291 
earths, basic, 277 

potassium urate, acid amorphous, 275 

pus in, 278, 282 

red corpuscles in, 281, 282 

renal casts in, 283. See also Renal casts, 

scheme for, 261-263 

soaps, 266 

sodium urate, acid. 273 

staining, 258 

starch in, features. 2S2 

sulphate of calcium, 266 
amorphous, 274 

triple phosphates, 271 
alkaline, 275 

tyrosin, 267, 268 

urates, acid ammonium, 272 
ammonium, alkaline, 276 
amorphous, 274 
calcium', acid amorphous, 275 
of sodium, acid, 273 
potassium, acid amorphous, 275 

uric acid, 264 

washing, 259 

xanthin, 272 

yeast-cells in, features, 282 
Uri4ie, 168 
acetic acid in, 250 
aceto-acetic acid in, 240 
acetone in, 240 
acidity of, 176 
actinomyces in, 301 
adenin in, 200 
after rhubarb, 256 
after senna, 256 
albumin in, 206. See also Albumin in 

loiiie. 
albumose in, 216. See also Albumose in 

urine. 
alkaline, 176 

amorphous deposits in, 277 

phosphates in, 181, 182 

sediments of, 275 

volatile, 177 
alkaloids in, 256 
alkapton in, 247 
alloxin bases in, 196, 200 
ammonia in, 177, 246 
ammoniomagnesium phosphates in, 271 
ammonium urates in, acid, 172 

alkaline. 276 
Amoeba urogenitalis in, 300 
amorphous deposits in, 274 
amphoteric, 177 
amyloid casts in, 289 
Anguillula aceti, 298 
animal parasites in, 292 

Stiles' key to, 299 
antifebrin in, 256 



INDEX. 



S6i 



Urine, aiitimon\' in, 256 
antipyrin in, 256 

color of, 171 
arabinose in, 238 
arsenic in, 256 
Ascaris lumbricoides in, 297 
aspergillus in, 301 

tumigatus in, 301 
Bacillus coli communis in, 307 

of diphtheria in, 306 

of glanders in, 306 

of Sternberg in, 306 

proteus vulgaris in, 307 

pyocyaneus in, 307 

tuberculosis in, 303, 307 

typhosus in, 305 
bacteria in, 301 

Bence-Jones' albumose in, 218 
bile in, 239 
bile-acid in, 239 
bilirubin crystals in, 270 
blood in, 170, 221, 281 
blood-casts in, 284, 287 
bloody, 170 

parasites in, 297 
boric acid crystals in, 267 
bothriocephalus liguloides in, 300 
bromin in, 256 
brown, 170 
butyric acid in, 250 
cadaverin in, 254 
calcium carbonate in, 277 

oxalate crystals in, 265 
amorphous, 274 

phosphate in, 182, 267 

soap in, 266 

sulphate crystals in, 266 
amorphous, 274 

urate in, acid amorphous, 275 
calculi in, 278 
cancer fragments in, 291 
carbohydrate in, 224 
carbolic acid in, 256 

gas in, 254 
carbonate of calcium in, 277 
casts in, 283. See also Reiial casts. 
centrifugal analysis of, 189 
centrifuge for, 257 
chemistry of, 177 
chlorids in, 179 

estimation of, centrifugal, 189 

phosphates and urea and, ratio, 193 

urea and phosphates and, ratio, 193 
cholesterin in, 245 
crystals in, 272 
chylous, 252, 253 
clap shreds in, 291 
clarification of, 236 
cloudy, 171 

colon bacillus in, 306, 307 
color of, 169-171 
composite casts in, 284, 289 
concretions in, 278 
conjugate sulphates in, 185 
consistence of, 172 
constituents of, 177 
cryoscopy of, deductive, 72 
crystals in, 260 
cystin in, 246, 271 
cylindroids in, 284, 290 
dark bodies in, 274 

dextrose in, 224, 239. See also Glucosuria. 
diabetic, 176 
diacetic acid in, 243 
diazo-reaction, Ehrlich's, 249 
dihydroxyphenylactic acid in, 247 
dimethylamidobenzaldehyd reaction with, 

Ehrlich's, 249 
diphtheria bacillus in, 306 
Diplococcus scarlatinEe in, 306 

36 



Urine, Distoma haematobium in, 295 
drugs and, 255 

earthy phosphates in, 181, 182 
echinococcus cysts in, 292 
Ehrlich diazo-reaction with , 249 

dimethylamidobenzaldehyd reaction 
with, 249 
electric conductivity of, 175 
epithelia in, 279, 282 
epithelial casts in, 2S8 
ethereal sulphates in, 185 
eustrongylus gigas in, 299 
false casts in, 284, 290 
fat in, 251, 274 
fatty acids in, volatile, 250 
fatty-acid casts in, 289 
fibrin in, 224 

Filaria sanguinis hominis in, 294 
fixed alkalis in, 177 
floaters in, 291 
formic acid in, 250 
fungi in, 300 
gases in, 254 
glanders bacillus in, 306 
globulin in, 206, 214 
glucose in, 224. See also Glucosuria. 
glycerin in, 531 
glycuronic acid in, 239 
gonococci in, 303, 497 
gratiular casts in, 284, 286 
grape sugar in, 224. See also Glucosuria. 
green, 170 

greenish-brown. 170 
greenish-yellow, 170 
guanin in, 200 
gum in, 239 
hematoidin casts in, 285 

crystals in, 270 
hematin in, 223 
hemoglobin in, 222 
heteroxanthin in, 196, 200 
hipputic acid in, 201 
hippuric-acid crystals in, 271 
histon in, 223 
hyaline casts in, 284, 285 
hydrochinon in, 256 
hydrogen sulphid in, 254 
hydroquinon in, 256 
hydroxybutyric acid in, 240 
hypoxanthin in, 200 
in diabetes, 182 

in endocarditis, ulcerative, 304 
in nephritis, 304 
indican in, 211, 538 
indigo in, 277 
infusoria in, 300 
inorganic sediments in, 260 
inosite in, 239 
iodid of potassium in, 256 
iodin in, 255 
kreatin in, 204 
lactic acid in, 244 
lactose in, 238 
laiose in, 239 
lead in, 256 

leucin crystals in, 267, 269 
leukocytes in, 278, 2S2 
levulose in, 239 
light in study of, 258 
Loffler bacillus in, 306 
microscopic appearance of. 168 
magnesium phosphate in, 1S2 

phosphates in, basic, 271 

soap in, 266 
maltose in, 239 
mercury in, 256 
metals in, 256 
methemoglobin in, 223 
microscopy of, 257 
milky, 252 
mineral ash in, 178 



c;62 



INDEX. 



L'rine, sulphates in, 185 
morphin in, 257 
mucin in, 205, 210, 215 
mucus in, 249 
naphthalin in, 256 
nitrogen in, 254 

secretion in, 192 

total, estimation, 195 
nucleo-albumin in, 210, 215 
odor of, 172 

org-anic sediments in, 278 
organized casts in, 2S4 
oxalate of calcium in, amorphous, 274 
oxalate-of-calcium cr>-3tals in, 265 
oxalic acid in, 203 
oxybutyric acid in, 242 
oxygen in, 254 

Oxyuris vermicularis in, 297 
parasites in, animal, 292 
Stiles' key to, 299 

vegetable, 300 
paraxanthin in, 200 

Parkes" classification of constituents of, 177 
pentoses in, 23S 
peptones in, 217 
phosphates in, 181 

alkaline, iSi, 1S2, 1S3 

ammoniomagnesium, 271 

centrifugal estimation, 190 

chlorids and urea and, ratio, 193 

earthy, iSr, 1S2 

of calcium in, 267 

of magnesia in, basic, 271 

triple, 271 
alkaline, 275 

urea and chlorids and, ratio, 193 
phosphacic earths in, basic, 277 
phosphoric acid in, iSi 

estimation, 1S4 
physical properties of, 168 
pigments of, 169, 210 
poisons in, 256 
potassium in, 177 

iodid in, 256 

urate in. acid amorphous, 275 
preformed sulphates in, 1S5 
propionic acid in, 250 
proteids in, 205 
ptomains in, 254 
purin bases in, 196, 200 

quantitative estimation, 529 
pus in, 246. 27S 

differentiation, 215 

features, 282 
pus-casts in, 288 ^ 
putrescin in, 254 
pyemia cocci in, 304 
pyknometer for specific gravity of, 213 
quantity of, 16S 
quinin and, 171, 256 
ray fungus in, 301 
reaction of, 176 
red, 171 

corpuscles in, 281, 2S2 
renal casts in, 283. See also Renai casts. 
resinous bodies in, 211 
resorcin in, 256 
rhabditis genitalis in, 297 
rhamnose in, 23S 
salicylates in, 256 
salicylic acid in, 256 
salol in, 256 
sarcolactic acid in, 244 
Schistosoma haematobium in, 295 
sedimentation of, 257 
sediments in, 257, 260. See also Urinary 

sedhnents. 
septicemia cocci in, 304 
serum-albumin in, 206. See also Albumin 

ill urine. 



Urine, serum-globulin in, 206, 214 
silver in, 256 
soaps in, 266 
sodium in, 177 

chlorid in, 179 
solids of, 174 
specific gravity of, 172 
pyknometer for, 213 
urinometer for, 174 
spermatozoa in, 291 
spirillum of relapsing fever in, 306 
Staphylococcus pyogenes albus in, 307 

aureus in, 307 
starch in, 253, 2S2 
Sternberg bacillus in, 306 
Streptococcus pyogenes erysipelatis in, 30^ 
strychnin in, 256 
sugar in. 224 
sulphates in, 1S5 

calcium, amorphous, 274 
crystals, 266 
estimation, centrifugal, 191 

ethereal, 1S5 

mineral, 185 

preformed, 1S5 
sulphonal and, color of, 171 
sulphur in, 1S5, 1S7 
sulphureted hydrogen in, 254 
sulphuric acid in, 1S5 
suppression of, 169 
syrupy, 172 

Tcenia echinococcus in, 292 
thallin in, 256 
transparency of. 171 
trichocephaius in, 419 

dispar in, 29S 
Trichomonas vaginalis in, 300 
triple phosphates in, 1S2, 271 

alkaline, 275 
tubercle bacillus in, 303, 307 
tumor fragments in. 291 
turbid, from urates, 171 
typhoid bacillus in, 305 
tyrosin crystals in, 267, 268 
unorganized casts in, 283 
urate casts in. 2S4 
urates in, acid ammonium, 272 

ammonium, alkaline, 276 

amorphous. 274 

Boston's test for, 210 

calcium, acid amorphous, 275 

potassium, acid amorphous, 275 
urea in. 192 
urein in, 24S 
uric acid in, 196. See also Uric acid iti 

iirine. 
uric-acid crystals in. 264 
vegetable parasites in, 300 
vinegar eel in. 29S 
volatile alkalis in, 177 

fatty acids in. 250 
waxy casts in, 289 
worms in, 292 

Stiles' key to, 299 
xanthin bases in. 200 

cr>-stals in, 272 
xylose in. 238 
yeast-cells in, features, 2S2 
jellow, 171 
Urinometer, Squibb's, 173 

Vaccinia, blood in, 137 

parasite of, 536 
Vagina, worms in. Stiles' key to, 299 
Vaginal gonorrhea, 4S3 
secretion, 481 
animal parasites in, 4S4 
bacteria in, 4S1, 4S2 
bactericidal properties of, 483 
Doderlein's bacillus in, 4S1 



INDEX. 



563 



Vaginal secretion, fungi in, 4S6 
in blennorrhea, 486 
in dysmenorrhea, 486 
in gestation, 483 
in mycosis, 4S6 
in pruritus vulvae, 486 
in vaginitis, 4S5 
in vulvitis, 485 
oxyurides in, 484 
parasites in, animal, 4S4 
Trichomonas vaginalis in, 484 
Vaginitis, discharge in, 485 
Valerian, alkaline phosphates in urine and, 183 
Valerianic acid in feces, 368 
Vera macaque, 514 
\'aricella, parasite of, 536 
\'ariola, parasite of, 536 
\'ibrio of cholera, Widal reaction and, 124 
Vincent's spirillum in saliva, 455, 456 
\'inegar eel in urine, 298 
\'olatile fatty acids in urine, 250 
Volhard's method for chlorids in urine, Sal- 

kovvski's modification, 180 
Volumetric estimation of albumin in urine, 

211 
Vomit, 352 
bile in, 334 
blood in, 354 
fecal, 354 
mucus in, 353 
odor, 352 
parasites in, 355 
pus in, 355 
saliva in, 353 
stercoraceous, 354 
time of, 352 
Von Fleischl's hemoglobinometer, 48-55 
Vulva, diphtheria of, 484 

noma of, 484 
Vulvitis, discharge in, 485 



Waldvogel's method of cryoscopy of blood, 

70 
Warm-water bath, 367 
Wash-bottle, 80 
Water in red cells, 83 



Water-motor centrifuge, 189 
Waxy casts in urine, 289 

Weber and Miiller test for blood in vomit, 354 
Weichselbaum's Diplococcus intracellularis 
in cerebrospinal fluid, 502 
in nasal secretion, 466 
Weights, 526 

Wetherill's color-scales, 524 
WetherilTs torfugation, 523, 528 * 
Weyl's test for kreatin in urine, 205 
Whetstone crystal, 264 

White corpuscles, 94. See also Leukocytes. 
Whooping-cough, blood in, 138 

protozoon in sputum, 436 
Widal reaction, 118, 124 

Wright's pipet for collecting blood for, iig 
Williamson's test for diabetes, 68 
Woodward's estimation of proteids in milk, 

522 
Worms in urine, 292 
Stiles' key to, 299 
screw, 513 
Wright's coagulometer, 41 
method for olood, 78 

for malarial parasites, 158 
pipet for collecting blood for Widal re- 
action, 119 
stain for blood, 79 



Xanthin base, 196 

electric conductivity of, 175 

in urine, 200 
crystals, 200 

in urine, 272 
Xylose in urine, 238 



Yeast-cells in urinary sediment, features, 

282 
Yeasts in sputum, 437 
Yellow fever, blood in, 139 



Zymogens of ferments, 335 



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PHYSIOLOGY. 13 



American Text- Book of Physiolog'y 



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be used independently of the practical exercises, which constitute an important 
feature of the book. In the present edition a considerable amount of new matter 
has been added, especially to the chapter on The Central Nervous System. 

Philadelphia Medical Journal 

" Those familiar with the attainments of Prof. Stewart as an origjinal investigator, as a 
teacher and a writer, need no assurance that in this volume he has presented in a terse, concise, 
accurate manner the essential and best established facts of physiology in a mob' attractive 
manner." 



14 



SAUNDERS' BOOKS ON 



Levy and Klemperer's 
Clinical Bacteriology 

The Elements of Clinical Bacteriology. By Drs. Ernst Levy and 
Felix Klemperer, of the University of Strasburg. Translated and 
edited by Augustus A. Eshner, M. D., Professor of Clinical Medicine, 
Philadelphia Polyclinic. Octavo volume of 440 pages, fully illustrated. 
Cloth, ^2.50 net. 

S. Solis-Cohen, M. D., 

Professor of Clinical Medicine, Jefferson Medical College, Philadelphia. 

" I consider it an excellent book. I have recomnmended it in speaking to my students." 

Lehmann, Neumann, and 
Weaver's Bacteriology 

Atlas and Epitome of Bacteriology : including a Text-Book of 
Special Bacteriologic Diagnosis. By Prof. Dr. K. B. Lehmann 
and Dr. R. O. Neumann, of Wiirzburg. From the Second Revised and 
Enlarged Ger^nan Edition. Edited, with additions, by G. H. Weaver, 
M. D., Assistant Professor of Pathology and Bacteriology, Rush Medical 
College, Chicago. In two parts. Part L — 632 colored figures on 69 
lithographic plates. Part II. — 511 pages of text, illustrated. Per part: 
Cloth, ;^2.50 net. In Saunders' Hand-Atlas Series. 

Lewis* Anatomy and Physi- 
ology for Nurses 

Anatomy and Physiology for Nurses. By LeRoy Lewis, M.D., 

Surgeon to and Lecturer on Anatomy and Physiology for Nurses at 

the Lewis Hospital, Bay City, Michigan. i2mo of 200 pages, with 

100 illustrations. 

JUST ISSUED 

The author has based the plan and scope of his work on the methods he has 
employed in teaching the subjects, and has made the text unusually simple and 
clear. The object was so to deal with anatomy and physiology that the student 
might easily grasp the primary principles, at the same time laying a broad foun- 
dation for wider study. 



PATHOLOGY, BACTERIOLOGY, AND PHYSIOLOGY. 



Senn'S Tumors second Revised Edition 

Pathology and Surgical Treatment of Tumors. By Nicholas 
Senn, M. D., Ph. D., LL.D., Professor of Surgery, Rush Medical Col- 
lege, Chicago. Handsome octavo, 718 pages, with 478 engravings, 
including 12 full-page colored plates. Cloth, ^5.00 net; Sheep or Half 
Morocco, $6.00 net. 

" The most exhaustive of any recent book in English on this subject. It is well illus- 
trated, and will doubtless remain as the principal monograph on the subject in our 
language for some ye3.TS."— Journal of the American Medical Association. 

Stoney's Bacteriology and Technic N^lT2dI Edmol, 

Bacteriology and Surgical Technic for Nurses. Bv Emily M. A. 
Stoney, Superintendent, Carney Hospital, Mass. Revised by Frederic 
R. Griffith, M.D., Surgeon, N. Y. i2mo of 278 pages, illustrated. 
$1.50 net. 

" These subjects are treated most accurately and up to date, without the superfluous 
reading which is so often employed. . . . Nurses will find this book of the greatest value." 
— The Trained Nurse and Hospital Review. 

Clarkson's Histology 

A Text-Book of Histology. Descriptive and Practical. For the 
Use of Students. By Arthur Clarkson, M. B., C. M. Edin., formerly 
Demonstrator of Physiology in the Owen's College, Manchester, Eng- 
land. Octavo, 554 pages, with 174 colored original illustrations. 
Cloth, $4.00 net. 

" The volume in the hands of students will greatly aid in the comprehension of a sub- 
ject which in most instances is found rather difficult. . . . The work must be considered 
a valuable addition to the list of available text-books, and is to be highly recommended.'' 
— New York Medical Journal. 

Gorham's Bacteriology 

A Laboratory Course in Bacteriology. For the Use of Medical, 
Agricultural, and Industrial Students. By Frederic P. Gorham, A. M., 
Associate Professor of Biology in Brown University, Providence, R. I., 
etc. i2mo of 192 pages, with 97 illustrations. Cloth, ^1.25 net. 

" One of the best students' laboratory guides to the study of bacteriology on the mar- 
ket. . . . The technic is thoroughly modern and amply sufficient for all practical pur- 
poses." — American Journal of the Medical Sciences. 

Raymond's Physiology Nei^sd) Ed^on 

Human Physiology. By Joseph H. Raymond, A. M., M. D., Pro- 
fessor of Physiology and Hygiene, Long Island College Hospital, New 
York. Octavo of 685 pages, with 444 illustrations. Cloth, ^3.50 net. 

"The book is well gotten up and well printed, and may be regarded as a trustworthy 
guide for the student and a useful work of reference for the genera: practitioner. The 
illustrations are numerous and are well executed." — The Lancet, London. 



i6 BACTERIOLOGY, PHYSIOLOGY, AND HISTOLOGY. 

Ball's Bacteriology Recently Issued— Fifth Edition, Revised 

Essentials of Bacteriology : being a concise and systematic intro- 
duction to the Study of Micro-organisms. By M. V. Ball, M. D., Late 
Bacteriologist to St. Agnes' Hospital, Philadelphia. i2mo of 236 pages, 
with 96 illustrations, some in colors, and 5 plates. Cloth, |i.oo net. In 
Saunders' Question- Co7Jipend Series. 

" The technic with regard to media, staining, mounting, and the like is culled from the 
latest authoritative works." — The Medical Times, New York. 

Budgett's Physiology 

Essentials of Physiology. Prepared especially for Students of Medi- 
cine, and arranged with questions following each chapter. By Sidney 
P. Budgett, M. D., Professor of Physiology, Medical Department of 
Washington University, St. Louis. i6mo volume of 233 pages, finely 
illustrated with many full-page half-tones. Cloth, $1.00 net. In 
Saunders' Question- Compend Series. 

" Contains the essential facts of physiology presented in a clear and concise manner." — 
Philadelphia Medical Journal. 

LerOy'S Histology second Edition, Revised 

Essentials of Histology. By Louis Leroy, M. D., Professor of 

Histology and Pathology, Vanderbilt University, Nashville, Tennessee. 

i2mo, 263 pages, with 92 original illustrations. Cloth, $1.00 net. In 

Saunders' Questioji- Co?npend Series. 

" The work in its present form stands as a model of what a student's aid should be ; and 
we unhesitatingly say that the practitioner as well would find a glance through the book 
of lasting benefit." — The Medical World, Philadelphia. 

Bastin's Botany 

Laboratory Exercises in Botany. By the late Edson S. Bastin, 
M. a. Octavo, 536 pages, with 87 plates. Cloth, $2.00 net. 

Barton and Wells' Medical Thesaurus 

A Thesaurus of Medical Words and Phrases. By Wilfred M. 
Barton, M. D., Assistant Professor of Materia Medica and Therapeutics, 
and Walter A. Wells, M.D., Demonstrator of Laryngology, Georgetown 
University, Washington, D. C. i2mo, 534 pages. Flexible leather, 
$2.50 net; thumb indexed, $3.00 net. 

American Pocket Dictionary ""RecentiTissue?""' 

Borland's Pocket Medical Dictionary. Edited by W. A. New- 
man Dorland, M. D., Assistant Obstetrician to the Hospital of the 
University of Pennsylvania. Containing the pronunciation and defini- 
tion of the principal words used in medicine and kindred sciences, with 
64 extensive tables. Handsomely bound in flexible leather, with gold 
edges, ^i.oo net; with patent thumb index, ^1.25 net. 

" I can recommend it to our students without reserve." — J. H. HOLLAND, M. D., Dean 
of the Jefferson Medical College, Philadelphia. 



SEP. 6 1905 



